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NO HYPE
07-01-2007, 12:45 PM
I just wanted to take a few minutes, not to discuss dementia as a disease, but to discuss the supplements which I have incorporated into my father's daily supplemental protocol, that have demonstrated unequivocal efficacy in the alleviation of his symptoms. Additionally in my opinion, I STRONGLY feel that these antioxidants when taken regularly, will significantly reduce the risk of developing this disease.

With the exception of alpha-synuclein accumulation and somatic dysfunction, inflammation and oxidation are the key physiological substrates underlying the progression of dementia.

The inhibition of oxidation and the attenuation of inflammation can be achieved (among other nutrients) via polyphenol antioxidants. Polyphenols have been found to effectively inhibit ROS (wich in excess, causes significant damage and/or death to cell structures) and peroxynitrite (one of the main mediator pro-inflammatory molecules).

Other non-polyphenol antioxidants that aquire the synergistic potential to accomplish the above mentioned tasks include: N-Acetyl-Cysteine, ALA, ubiquinol/idebenone, curcumin, selenium, fish oil, vitamin C, vitamin A, vitamin E, melatonin, ect. These antioxidants will also assist in inhibiting excessive cytochrome P450-induced, free radical cell damage.

For those of you with family or friends who suffer from this nightmare, one thing that is important to keep in mind when contemplating a nutritional approach to improve conditions.... neuronal damage can be lessened, however nothing can be done for the neuronal death that has already occurred. Unfortunately that's a void that will never be filled.

Fortunately, I started him on this protocol shortly after I found out he had dementia (although I can't stress enough, the fact that I would give anything to have known of this information PRIOR to finding out). Throughout the timespan of about 10 months, I have literally witnessed a DRAMATIC, visible transformation in physical appearance, cognitive function, and overall way of life.

I truly hope that this information reaches anyone who is unaware of these facts.

NO HYPE
07-01-2007, 12:46 PM
On a side note, I am in need of Steve from Unique Nutrition to share his OPINION on the possible use of nootropics, to ameliorate the symptoms of congnitive decline in dementia. If you are reading this Steve, the following applies....


In your OPINION Steve, with dosages being taken twice a day for cholinesterase/neuroinflammation inhibition, what size of a dosage of huperzine A would be ideal?

Also in relation to nootropics, do you have any other suggestions for this disease? I've got my dad on huperzine A, picamilon, and CDC choline (as well as 5-HTP).

He is responding well at a dosage of 2 capsules of huperzine 2x a day, and 1 capsule of picamilon/choline 2x a day.

It seems as though the aniracetam has a stimulatory effect, which seems to upregulate hallucinations.... but this will require more attention before I come to a definitive conclusion.

stoptherun51
07-01-2007, 12:49 PM
nice post. a good read^^

I didnt think simple otc antiox could have effects on something as dibilitating as dimentia

NO HYPE
07-01-2007, 12:50 PM
nice post. a good read^^

I didnt think simple otc antiox could have effects on something as dibilitating as dimentia

Thanks... reps to you.

CognitiveNutrition
07-01-2007, 01:22 PM
On a side note, I am in need of Steve from Unique Nutrition to share his OPINION on the possible use of nootropics, to ameliorate the symptoms of congnitive decline in dementia. If you are reading this Steve, the following applies....


In your OPINION Steve, with dosages being taken twice a day for cholinesterase/neuroinflammation inhibition, what size of a dosage of huperzine A would be ideal?

Also in relation to nootropics, do you have any other suggestions for this disease? I've got my dad on huperzine A, picamilon, and CDC choline (as well as 5-HTP).

He is responding well at a dosage of 2 capsules of huperzine 2x a day, and 1 capsule of picamilon/choline 2x a day.

It seems as though the aniracetam has a stimulatory effect, which seems to upregulate hallucinations.... but this will require more attention before I come to a definitive conclusion.


Previous AD research with L-Huperzine A used 400 mcg daily the current US study is going as high as 800 mcg. I would suggest 400 mcg give no other potent ACh compound is given. (1)

Picamilon is weakly research for AD sad to say. (While it may be helpful no research I'm aware of confirms it).

CDP-Choline is well studied in AD and I would highly recommend it. (2)

Racetams while showing various neuroprotective effects have minimal impact on disease symptoms or progressive. However I do believe racetams can be a helpful add on due to the available research. (3)

For inflammation I would suggest EPA/DHA, sesamin, curcumin, and 5-Loxin. Which target a few pathways (COX, NF-κB , LOX, ).

Carnosine I would recommend due to the animal research and it?s unique effects on glycation as a possible cofactors in worsening the condition (Do a pubmed search carnosine + dementia).

Methyl B-12 , Pyritinol, vincamine, Hydergine and Idebenone has some positive clinical research in AD as well and should be considered. (4, 5, 6)


(1) http://www.mindandmuscle.net/forum/index.php?showtopic=27521
(2) http://www.mindandmuscle.net/forum/index.php?showtopic=27526
(3) http://www.mindandmuscle.net/forum/index.php?showtopic=27519
(4) http://www.mindandmuscle.net/forum/index.php?showtopic=27524
(5) http://www.mindandmuscle.net/forum/index.php?showtopic=27529
(6) http://www.mindandmuscle.net/forum/index.php?showtopic=29408

NO HYPE
07-01-2007, 01:28 PM
Previous AD research with L-Huperzine A used 400 mcg daily the current US study is going as high as 800 mcg. I would suggest 400 mcg give no other potent ACh compound is given. (1)

Picamilon is weakly research for AD sad to say. (While it may be helpful no research I'm aware of confirms it).

CDP-Choline is well studied in AD and I would highly recommend it. (2)

Racetams while showing various neuroprotective effects have minimal impact on disease symptoms or progressive. However I do believe racetams can be a helpful add on due to the available research. (3)

For inflammation I would suggest EPA/DHA, sesamin, curcumin, and 5-Loxin. Which target a few pathways (COX, NF-κB , LOX, ).

Carnosine I would recommend due to the animal research and it?s unique effects on glycation as a possible cofactors in worsening the condition (Do a pubmed search carnosine + dementia).

Methyl B-12 , Pyritinol, vincamine, Hydergine and Idebenone has some positive clinical research in AD as well and should be considered. (4, 5, 6)


(1) http://www.mindandmuscle.net/forum/index.php?showtopic=27521
(2) http://www.mindandmuscle.net/forum/index.php?showtopic=27526
(3) http://www.mindandmuscle.net/forum/index.php?showtopic=27519
(4) http://www.mindandmuscle.net/forum/index.php?showtopic=27524
(5) http://www.mindandmuscle.net/forum/index.php?showtopic=27529
(6) http://www.mindandmuscle.net/forum/index.php?showtopic=29408


Thank you Steve, for contributing such invaluble information to this thread. I will review the links that you've posted in their entirety.

BB.com is fortunate to have you on board.

.

CognitiveNutrition
07-01-2007, 02:42 PM
Thank you Steve, for contributing such invaluble information to this thread. I will review the links that you've posted in their entirety.

BB.com is fortunate to have you on board.

.

I can have our M.D. forward me his protocol for dementia if you're interested. Do you know what type he has, what stage, and what if any drugs he is on now? Plus any other health issues?

Your welcome I got involved in this because I want to give people a choice and options for their health.

DRP7
07-01-2007, 02:56 PM
I just wanted to take a few minutes, not to discuss dementia as a disease, but to discuss the supplements which I have incorporated into my father's daily supplemental protocol, that have demonstrated unequivocal efficacy in the alleviation of his symptoms. Additionally in my opinion, I STRONGLY feel that these antioxidants when taken regularly, will significantly reduce the risk of developing this disease.

With the exception of alpha-synuclein accumulation and somatic dysfunction, inflammation and oxidation are the key physiological substrates underlying the progression of dementia.

The inhibition of oxidation and the attenuation of inflammation can be achieved (among other nutrients) via polyphenol antioxidants. Polyphenols have been found to effectively inhibit ROS (wich in excess, causes significant damage and/or death to cell structures) and peroxynitrite (one of the main mediator pro-inflammatory molecules).

Other non-polyphenol antioxidants that aquire the synergistic potential to accomplish the above mentioned tasks include: N-Acetyl-Cysteine, ALA, ubiquinol/idebenone, curcumin, selenium, fish oil, vitamin C, vitamin A, vitamin E, melatonin, ect. These antioxidants will also assist in inhibiting excessive cytochrome P450-induced, free radical cell damage.

For those of you with family or friends who suffer from this nightmare, one thing that is important to keep in mind when contemplating a nutritional approach to improve conditions.... neuronal damage can be lessened, however nothing can be done for the neuronal death that has already occurred. Unfortunately that's a void that will never be filled.

Fortunately, I started him on this protocol shortly after I found out he had dementia (although I can't stress enough, the fact that I would give anything to have known of this information PRIOR to finding out). Throughout the timespan of about 10 months, I have literally witnessed a DRAMATIC, visible transformation in physical appearance, cognitive function, and overall way of life.

I truly hope that this information reaches anyone who is unaware of these facts.


what kind of dementia does he have?

NO HYPE
07-01-2007, 05:08 PM
any other health issues?

Not so much since the inclusion of supplemental nutrients, but one inhibiting factor in relation to his overall health, is a lack of exercise.

I am curious as to the condition of the kidneys/liver due to the peripheral edema of the legs that he experienced prior to supplementation. He also had high blood pressure, but that has pretty much been corrected. We'll see this week when he goes for his check-up.

NO HYPE
07-01-2007, 05:11 PM
Do you know what type he has, what stage, and what if any drugs he is on now?


what kind of dementia does he have?

He has DLB (Dementia with Lewy Bodies). He was diagnosed about a year ago, however there were indications that something was possibly wrong, for about 6 months prior (i.e. losing balance, forgeting common tasks, ect.). The progression was slow at first, but right around the time he was diagnosed, it worsened and he began experiencing frequent hallucinations, followed by autonomic dysfunction.

This is around the time when doctors were attempting the pharmaceutical approach (i.e. quetiapine fumarate-100mg daily, followed by a short trial of Donepezil-5mg), but to no avail. In fairness to the effectiveness of the acetyl cholinesterase inhibitors though, my mother did not feel comfortable with the whole "drug" approach (as his conditions appeared to worsen), so we just stopped treatment altogether.

During this time, the disease quickly caused his posture to almost completely give way. This eventually resulted in his inabillity to walk without the assistance of a walker. Every simple task became his worst nightmare (and mine too).

This is when I decided enough was enough. Here's the kicker....

I started him on the above-mentioned protocol (along with other supplemental nutrients), and within about 3-4 WEEKS, he was walking WITHOUT the walker, his posture had SIGNIFICANTLY improved, the severity of autonomic dysfunction had lessened, and the tasks that were a nightmare in previous weeks soon became simple once again.

NO HYPE
07-01-2007, 05:16 PM
I can have our M.D. forward me his protocol for dementia if you're interested.

Thank you Steve.

I'd very much like to compare it to my own. Any suggestions from knowledgable people on the matter, are more than welcomed.

DRP7
07-01-2007, 05:33 PM
He has DLB (Dementia with Lewy Bodies). He was diagnosed about a year ago, however there were indications that something was possibly wrong, for about 6 months prior (i.e. losing balance, forgeting common tasks, ect.). The progression was slow at first, but right around the time he was diagnosed, it worsened and he began experiencing frequent hallucinations, followed by autonomic dysfunction.

This is around the time when doctors were attempting the pharmaceutical approach (i.e. quetiapine fumarate-100mg daily, followed by a short trial of Donepezil-5mg), but to no avail. In fairness to the effectiveness of the acetyl cholinesterase inhibitors though, my mother did not feel comfortable with the whole "drug" approach (as his conditions appeared to worsen), so we just stopped treatment altogether.

During this time, the disease quickly caused his posture to almost completely give way. This eventually resulted in his inabillity to walk without the assistance of a walker. Every simple task became his worst nightmare (and mine too).

This is when I decided enough was enough. Here's the kicker....

I started him on the above-mentioned protocol (along with other supplemental nutrients), and within about 3-4 WEEKS, he was walking WITHOUT the walker, his posture had SIGNIFICANTLY improved, the severity of autonomic dysfunction had lessened, and the tasks that were a nightmare in previous weeks soon became simple once again.



hmmm. normaly, DLB actually responds pretty well to AChE-Inhibitors. much better than Alzeheimer's Dementia.

quetiapine is solely for the hallucinations will do jack for the dementia as such.

are the hallucinations auditory or visual?
which symptoms predominate in the cognitive domain? visual(can't find the way, can't draw etc.) or memory (can't memorize new things) or speech-related (can't find the correct words) or is it apraxia (e.g. can't do easy things like using fork and knife)?
does he have tremor? are his muscles stiff?
did he use any anti-parkisnonian medicine?
was the diagnosis based solely on the clinical symptoms or did they do some sort of neuroimaging (PET, MRI)?
liquor-punction?

very important: have a brain-tumor (hallucinations, posture) and a normal-pressure-hydrocephalus (posture, walking, autonomic dysfunction, dementia) been excluded?

ab-swing asianbabe
07-01-2007, 05:55 PM
I can have our M.D. forward me his protocol for dementia if you're interested. Do you know what type he has, what stage, and what if any drugs he is on now? Plus any other health issues?

Your welcome I got involved in this because I want to give people a choice and options for their health.

I would love to see that, thanks Steve.

NO HYPE
07-01-2007, 06:18 PM
hmmm. normaly, DLB actually responds pretty well to AChE-Inhibitors. much better than Alzeheimer's Dementia.

I am not sold on the idea that they did not work, hence the reason I am reinstating cholinesterase inhibition by means of huperzine A. So far (2 weeks in), he is responding well.




are the hallucinations auditory or visual?

Both.




which symptoms predominate in the cognitive domain? visual(can't find the way, can't draw etc.) or memory (can't memorize new things) or speech-related (can't find the correct words) or is it apraxia (e.g. can't do easy things like using fork and knife)?



I'd say the following two....

visual (can't find the way, can't draw etc.)

speech-related (can't find the correct words)




does he have tremor?

Not regularly, but sometimes yes. This seems to dependant on factors such as the amount of exercise that he gets (i.e. when he increases physical activity, it seems to worsen).




are his muscles stiff?

Yes. More so from the torso to the neck. In fact, for a while prior to correcting the problem, I would regularly see him laying on his bed with his neck raised off the pillow.




did he use any anti-parkisnonian medicine?

No.




was the diagnosis based solely on the clinical symptoms or did they do some sort of neuroimaging (PET, MRI)?

I believe the diagnosis included MRI.

DRP7
07-01-2007, 06:24 PM
hmmm... the predominance of visual cognitive symptoms + hallucinations + extrapyramidal motor symptoms speaks in favour of DLB. the verbal symptoms are not so typical, however.

do the symptoms show large fluctuations? i.e. is he on some days much better than on others?

NO HYPE
07-01-2007, 10:46 PM
hmmm... the predominance of visual cognitive symptoms + hallucinations + extrapyramidal motor symptoms speaks in favour of DLB. the verbal symptoms are not so typical, however.

I must point out the fact that in terms of speech, it's not a severe and constant problem, it's more of a lack of volume and an occasional mispronunciation.




do the symptoms show large fluctuations? i.e. is he on some days much better than on others?

The symptoms certainly used to vary greatly (prior to the protocol), but the fluctuations are not as dramatic now. Sometimes though, towards the end of the day, he gets exhausted (especially after physical labor) and it sometimes worsens. Which brings me back to your previous question reguarding tremors.

I totally forgot about the fact that his tremors relate to his inibility to properly walk and function (sometimes it's only for a few seconds). These symptoms do not occur that often but what I have noticed is that when he has missed a day's worth of supplementation, they rapidly return.

DRP7
07-02-2007, 12:12 AM
I must point out the fact that in terms of speech, it's not a severe and constant problem, it's more of a lack of volume and an occasional mispronunciation.





The symptoms certainly used to vary greatly (prior to the protocol), but the fluctuations are not as dramatic now. Sometimes though, towards the end of the day, he gets exhausted (especially after physical labor) and it sometimes worsens. Which brings me back to your previous question reguarding tremors.

I totally forgot about the fact that his tremors relate to his inibility to properly walk and function (sometimes it's only for a few seconds). These symptoms do not occur that often but what I have noticed is that when he has missed a day's worth of supplementation, they rapidly return.

you are certainly on the right track with the antioxidants.

unfortunately, alpha-synuclein (which is the main constituent of lewy bodies)research is pretty much still in its children's shoes when compared to beta-amyloid research (in AD).

nonetheless, there are certain overlaps between DLB and AD pathology, so it surely would not hurt to recommend some things that have been shown to have beneficial effects on Amyloid production and/or clearance in AD:

- DHA (not EPA!)
- curcumin
- green tea

also, the role of mitochondrial dysfunction and insulin sensitivity are issues that are "hot-topics" in current AD-research. So, it would be worth to try supplements that improve both pathways.

I feel with you, NO HYPE and wish you really the best for you and your father / family. you are doing good and fortunately, your father actually takes the supps you give to him. there are many people who are too stubborn and don't take any advice, at least from their family members.

pesonally, I would try some resveratrol. this is THE cell rejuvenation substance par excellance!

you could dissolve it in oil and a tiny bit of lecithin and then apply it intranasally. (there are also some other solvants taht are used for this applicatino). BTW: the intranasal pathaway leads directly to the brain. try to do this with as many supps you can. I would recommend you to go to a good pharmacist and to ask him to make such special delivery preparations for you. the intranasal application is of course limited and should only augment the oral use.

best regards!

NO HYPE
07-02-2007, 04:18 AM
you are certainly on the right track with the antioxidants.

unfortunately, alpha-synuclein (which is the main constituent of lewy bodies)research is pretty much still in its children's shoes when compared to beta-amyloid research (in AD).

nonetheless, there are certain overlaps between DLB and AD pathology, so it surely would not hurt to recommend some things that have been shown to have beneficial effects on Amyloid production and/or clearance in AD:

- DHA (not EPA!)
- curcumin
- green tea

also, the role of mitochondrial dysfunction and insulin sensitivity are issues that are "hot-topics" in current AD-research. So, it would be worth to try supplements that improve both pathways.

I feel with you, NO HYPE and wish you really the best for you and your father / family. you are doing good and fortunately, your father actually takes the supps you give to him. there are many people who are too stubborn and don't take any advice, at least from their family members.

pesonally, I would try some resveratrol. this is THE cell rejuvenation substance par excellance!

you could dissolve it in oil and a tiny bit of lecithin and then apply it intranasally. (there are also some other solvants taht are used for this applicatino). BTW: the intranasal pathaway leads directly to the brain. try to do this with as many supps you can. I would recommend you to go to a good pharmacist and to ask him to make such special delivery preparations for you. the intranasal application is of course limited and should only augment the oral use.

best regards!

I am VERY much curious as to what you have to say about avoiding EPA, especially when considering it's effectiveness at inhibiting F2-isoprostane formation.

Isofurans, but not F2-isoprostanes, are increased in the substantia nigra of patients with Parkinson's disease and with dementia with Lewy body disease. (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12694390)


I thank you Dr.P and Steve, for your invaluble contribution to this thread.

DRP7
07-02-2007, 04:40 AM
I am VERY much curious as to what you have to say about avoiding EPA, especially when considering it's effectiveness at inhibiting F2-isoprostane formation.

Isofurans, but not F2-isoprostanes, are increased in the substantia nigra of patients with Parkinson's disease and with dementia with Lewy body disease. (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12694390)


I thank you Dr.P and Steve, for your invaluble contribution to this thread.

well, I haven't said to explicitely avoid EPA, I only said that DHA has been found to positively affect certain factors of amyloid pathology in AD while EPA has not been found to have these effects.

Too bad we are speaking about DLB where MUCH less information on underlying pathophysiology is available than in AD....:(

Skigazzi
07-02-2007, 07:55 AM
Great thread, great info.

With most of americans (me included) in the 20-50 age range having one of the primary concerns being how to deal with aging parents, this is a great thread.

I wish you and your father the best of luck in the future.

Bane
07-02-2007, 08:21 AM
I think you are forgeting the most important, gingko biloba, only antioxidant proven to bypass BBB and ameliorate nerve cell damage.
I don't know what happens in USA, in Greece however piracetam is often prescriebed for dementia and results i have seen have been very good.

NO HYPE
07-02-2007, 04:53 PM
well, I haven't said to explicitely avoid EPA, I only said that DHA has been found to positively affect certain factors of amyloid pathology in AD while EPA has not been found to have these effects.

Got ya.




Too bad we are speaking about DLB where MUCH less information on underlying pathophysiology is available than in AD....:(

This is unfortunately true. For example, in Parkinson's Disease, microglial EP2 is responsible for the majority of alpha-synuclein-mediated neurotoxicity. Does the same apply to dementia? If not, why not? These type of questions require MUCH more research.

NO HYPE
07-02-2007, 05:09 PM
Great thread, great info.

With most of americans (me included) in the 20-50 age range having one of the primary concerns being how to deal with aging parents, this is a great thread.

I wish you and your father the best of luck in the future.

Thank you kind sir.

NO HYPE
07-02-2007, 05:14 PM
I think you are forgeting the most important, gingko biloba, only antioxidant proven to bypass BBB and ameliorate nerve cell damage.
I don't know what happens in USA, in Greece however piracetam is often prescriebed for dementia and results i have seen have been very good.

You were right.... I totally forgot about ginko, and I'll give it a try. I haven't brushed up on that one in ages though, and I'm curious to view some in vivo studies. Thank you Bane.

NO HYPE
07-02-2007, 05:16 PM
inflammation and oxidation are the key physiological substrates underlying the progression of dementia.

The inhibition of oxidation and the attenuation of inflammation can be achieved (among other nutrients) via polyphenol antioxidants. Polyphenols have been found to effectively inhibit ROS (wich in excess, causes significant damage and/or death to cell structures) and peroxynitrite (one of the main mediator pro-inflammatory molecules).

Other non-polyphenol antioxidants that aquire the synergistic potential to accomplish the above mentioned tasks include: N-Acetyl-Cysteine, ALA, ubiquinol/idebenone, curcumin, selenium, fish oil, vitamin C, vitamin A, vitamin E, melatonin, ect. These antioxidants will also assist in inhibiting excessive cytochrome P450-induced, free radical cell damage.

For anyone reading who has family undergoing this disease. I really want to stress the importance of attenuating inflammation, and oxidative damage. Alpha-synuclein accumulation is cytotoxic, and induces neuroinflammation. This results in the progression of dementia, and the worsening of it's symptoms. Which brings me to my next point....


I hope you all realize just how important antioxidants are?

Does the phrase.... "hereditary alpha-synucleinopathies" mean anything to you? It does to me, and I'll be damned if I'm going to just sit back and let oxidative damage take it's toll, and ruin my life like it did my father's. Nope, no way.

in10city
07-02-2007, 05:34 PM
For anyone reading who has family undergoing this disease. I really want to stress the importance of attenuating inflammation, and oxidative damage. Alpha-synuclein accumulation is cytotoxic, and induces neuroinflammation. This results in the progression of dementia, and the worsening of it's symptoms. Which brings me to my next point....


I hope you all realize just how important antioxidants are?

Does the phrase.... "hereditary alpha-synucleinopathies" mean anything to you? It does to me, and I'll be damned if I'm going to just sit back and let oxidative damage take it's toll, and ruin my life like it did my father's. Nope, no way.
Serious... hope these work well for your father...

Would all of these supplemental mitigation approaches (inflammation and ROS control) be applicable across the board of dementia types - i.e. vascular / stroke related dementia?

NO HYPE
07-02-2007, 06:15 PM
Serious... hope these work well for your father...

Thank you (this approach has worked wonders so far).




Would all of these supplemental mitigation approaches (inflammation and ROS control) be applicable across the board of dementia types - i.e. vascular / stroke related dementia?

IMO.... to some degree yes.

I strongly feel that any neuroinflammative/neurodegenerative condition can be significantly improved via this approach.

in10city
07-02-2007, 06:32 PM
Thank you (this approach has worked wonders so far).

IMO.... to some degree yes.

I strongly feel that any neuroinflammative/neurodegenerative condition can be significantly improved via this approach.
Thanks... I have numerous relatives suffering from this type of dementia ... but I have one uncle who is doing remarkably well for himself ... the one thing that differentiates him from the others is the shear number and amount of "supplements" he takes (it would put anyone on the boards to shame really) ... I've never asked him nor dug through them to find out what they are, but I think I will next time...

NO HYPE
07-02-2007, 07:33 PM
Thanks... I have numerous relatives suffering from this type of dementia ... but I have one uncle who is doing remarkably well for himself ... the one thing that differentiates him from the others is the shear number and amount of "supplements" he takes (it would put anyone on the boards to shame really) ... I've never asked him nor dug through them to find out what they are, but I think I will next time...

Good luck with that.

One thing that I wanted to point out, is that when it comes to oral supplementation for improving symptoms of dementia.... a slow, yet steady flow of nutrients seems to be the most efficient delivery method for physiological uptake. This also greatly reduces the risk of any prooxidant damage triggered by large doses of combined nutrients.

Note: avoid administering vitamin C and NAC simultaneously during inflammatory response as it may promote hydroxyl radical formation in the presence of iron (Fe2+).

oziem
07-02-2007, 07:55 PM
There is some thinking that liver heavy metal toxicity is a culprit so a cleansing may be in order.
Fatty acids and vitamins are key for brain health.

eldawg
07-02-2007, 08:11 PM
Sorry this isn't a link to a study, but I was reading this article on BB.com and came across the reference to dememtia. May be worthwhile checking into it more:


Used and proven effective for over 20 years in Europe as a treatment for fatigue and dementia (dementia is a mental disorder that affects your ability to think, speak and move), Citrulline Malate (CM) has made its way into the western world in the arena of athletic performance nutrition.
http://www.bodybuilding.com/fun/jrod4.htm

NO HYPE
07-03-2007, 03:46 AM
There is some thinking that liver heavy metal toxicity is a culprit so a cleansing may be in order.
Fatty acids and vitamins are key for brain health.

Thank you.



These antioxidants will also assist in inhibiting excessive cytochrome P450-induced, free radical cell damage.

^^^^ This is the reason I regularly have him administer NAC, silymarin, ALA, ect. ^^^^

NO HYPE
07-03-2007, 03:51 AM
Sorry this isn't a link to a study, but I was reading this article on BB.com and came across the reference to dememtia. May be worthwhile checking into it more:


http://www.bodybuilding.com/fun/jrod4.htm

I was VERY recently, considering the inclusion of CM (along with creatine) to this protocol.

Thank you eldawg. :)

Bane
07-03-2007, 07:13 AM
You were right.... I totally forgot about ginko, and I'll give it a try. I haven't brushed up on that one in ages though, and I'm curious to view some in vivo studies. Thank you Bane.

There are. Back when i was looking in antioxidants gingko was the only one i found that could affect the brain. A quick search in pubmed brings up these:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=14753460&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11450097&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2947088&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17443523&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17341003&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum

There are more if you search
I am pretty sure i have the full studies somewhere, i'll see what i can do.

CognitiveNutrition
07-03-2007, 07:17 AM
Hey NO HYPE

I pm'ed you his reply fyi!

NO HYPE
07-03-2007, 01:07 PM
There are. Back when i was looking in antioxidants gingko was the only one i found that could affect the brain. A quick search in pubmed brings up these:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=14753460&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11450097&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2947088&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17443523&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17341003&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum

There are more if you search
I am pretty sure i have the full studies somewhere, i'll see what i can do.

Cool.... thanks B.

I truly appreciate it. Don't worry about the full versions (I can probably find them "IF" necessary).

NO HYPE
07-03-2007, 01:10 PM
Hey NO HYPE

I pm'ed you his reply fyi!

Thank you kindly.

NO HYPE
07-03-2007, 01:33 PM
Below is an excerpt from the PM that I recieved from Steve at Unique Nutrition.

Take your antioxidant folks!



Short Description

Dementia with Lewy bodies is a neurodegenerative disorder which displays pathological symptoms similar to Alzheimer's disease and Parkinson's disease.

Neurodegradation occurs in the nigrostriatal system, limbic-neocortical system, and peripheral autonomic nervous system. Largely affected are the cholinergic & dopaminergic systems resulting in impaired cognitive and motor functioning.

Decreased glucose metabolic reductions in the temporal, parietal, and frontal areas--including in the occipital lobe are important to note.

Abnormal alpha-synuclein (a neural protein) buildup is a major factor in neurodegeneration. Oxidative stress and inflammation accelerate this process.

Lee Crost M.D.


J Neurosci. 2007 Feb 7;27(6):1405-10
Acc Chem Res. 2006 Sep;39(9):611-9.

NO HYPE
07-03-2007, 03:05 PM
To anyone with a REM sleep behavior disorder, please pay close attention to this article and get yourself some melatonin. I can honestly tell you that this sleep disorder was a prominent issue for many years prior to my father developing dementia.... If only I had known!


September 01, 2006

REM Sleep Behavior Disorder: Harbinger of Synucleinopathies?
Charles J. Ippolito, MD


An unfavorable prognosis may be in store for patients who report severely disrupted sleep patterns accompanied by rapid eye movement (REM). Typically, these patients-mostly older men (80% to 90%)-thrash, strike out aggressively, and shout as if acting out their dreams, and they also vividly recall their dreams when awakened.1 The diagnosis is REM sleep behavior disorder (RBD), a parasomnia characterized by loss of normal sleep atonia during REM accompanied by prominent motor activity and dreaming. Because neurodegenerative diseases-specifically synucleinopathies such as Lewy body dementia (LBD), Parkinson disease (PD), and multiple system atrophy (MSA)-develop in many patients with RBD, these diseases and RBD and are thought to have a common pathogenesis. Indeed, RBD may be prognostic for the development of these neurodegenerative diseases.2,3

Findings from a retrospective study published in the July 2006 issue of Lancet Neurology revealed that a neurodegenerative disorder developed in 45% of patients (20 of 44) a mean of 11.5 years after RBD symptom onset.4 PD was diagnosed in 20% of patients, LBD in 14%, and MSA in 2%. In addition to concluding that RBD may be a harbinger of neurodegenerative disorders, the study's authors commented that close follow-up of affected patients could enable early detection of neurologic problems.

Important diagnostic features of RBD include complex vigorous movements of the body or limbs or excessive jerking, vivid recollection of dream content, and polysomnographic evidence of increased submental or limb tone (phasic or tonic) based on electromyography during REM sleep.5

Motor symptoms of RBD include kicking, punching, and crying out, all of which suggest degeneration of the nuclei in the pontine tegmentum and medulla. Neuronal deposition of alpha-nuclein proteins, a hallmark of LBD, PD, and MSA, appears to play a role.6


RBD AND SYNUCLEINOPATHIES

RBD is strongly linked to the synucleinopathies,7,8 which are insidious: these disorders can emerge years and even decades before characteristic parkinsonian symptoms or cognitive impairments manifest.7 Alpha-nuclein, an aggregated protein consisting of 140 amino acids, pervades brain tissue, is concentrated at presynaptic terminals, and is extensively nitrated in the brains of persons with PD, LBD, and MSA.

In MSA, the oligodendroglial inclusion bodies are the most distinctive neuropathologic feature. The formation of these inclusion bodies may explain the selective loss of oligodendroglia and of neurons. The inability of the oligodendrocytes to degrade alpha-nuclein proteins, which they produce at low levels, may be responsible for the abnormal subcellular aggregation and clumping found in MSA.1

Bradley F. Boeve, MD, associate professor of neurology and chair of the Division of Behavioral Neurology at the Mayo Clinic in Rochester, Minnesota, and colleagues have done much work to demonstrate that RBD is associated with PD, MSA, LBD, frontotemporal dementia, primary progressive aphasia, and spinocerebellar atrophy type 3, as well as certain tauopathies, including supranuclear palsy and Pick disease.8

Their studies show that a common characteristic of neurodegenerative diseases in persons with RBD is the presence of alpha-synuclein-positive intracellular inclusion bodies.8 These findings suggest that RBD may be symptomatic of an underlying synucleinopathy. The researchers noted that RBD does not appear to be associated with Alzheimer disease (AD) except in complex cases in which Lewy bodies are present.

"A remarkably consistent observation over the years is that RBD is a precursor to neurodegenerative diseases such as PD, LBD, and MSA. Of course, RBD is not present in all patients with synucleinopathies, but it is common, and it is rarely associated with tauopathies," explained Boeve in an interview with Applied Neurology.

"There is a clear linkage between neurodegenerative disease and the synucleinopathies," agreed David G. Harper, PhD, associate director of geriatric research at McLean Hospital in Belmont, Massachusetts. "What we should focus on here is the pattern of the damage seen in PD, MSA, and LBD compared with that of the tauopathies, such as AD and progressive supranuclear palsy. The alpha-synuclein proteins seem to aggregate in the neurons, particularly in PD and LBD, and in high concentrations in the substantia nigra."


RBD, PD, AND LBD

Many patients in whom either PD or LBD is newly diagnosed have a history of RBD.6,9 "Five years after seeking medical help for RBD symptoms, 45% of elderly patients progress to either PD or LBD," Harper remarked. Incidence of RBD has been reported at 15% to 33% in cases of PD,10 and Boeve and coworkers found Lewy body pathology in 83% (15 of 18) of autopsy cases of patients with RBD and dementia in the absence of parkinsonian symptoms.8

A proposed explanation for RBD in association with LBD is the loss of neurons in monoaminergic brain stem nuclei-particularly those in the locus coeruleus and substantia nigra-that causes decreased inhibition of the cholinergic pedunculopontine nucleus, which is the mediator of sleep atonia. In addition to being a useful treatment for LBD, cholinesterase inhibitors have been shown to reduce symptoms of RBD in some patients.9


RBD AND MSA

REM sleep without atonia, a variant of normal sleep in which muscle tone is present during REM, was first reported in patients with MSA in the 1970s.11 During the ensuing 3 decades, the association with its pathologic variant-RBD-and MSA has become firmly established. The distribution of neurodegeneration is generally more widespread in MSA than it is in PD, and it is generally characterized by atrophy of the pontine structures that are responsible for the phenomenon of REM-sleep muscle atonia.11 The most important early discriminator between MSA and PD is the poor response to levodopa in patients with MSA. These patients, mostly female, often exhibit disrupted sleep with REM phase alterations and may present with frank RBD.1


TREATMENT STRATEGIES

RBD may well become a bellwether for identifying patients before neurodegenerative motor symptoms develop, thus potentially allowing for early intervention in neurodegenerative disease,11 although preventive treatments for RBD and synucleinopathies currently are lacking.

"At this point, we unfortunately do not have any available treatments that will delay the onset or prevent the progressive degeneration related to the synucleinopathies,"explained Boeve. "Coenzyme Q10, a rather benign over-the-counter preparation, has been found to slow the rate of progression of RBD to PD. There is no actual proof that coenzyme Q10 works, but since it requires no prescription, it is an agent that people with idiopathic RBD might try. Unfortunately, no proper dosage has been established."

"Worldwide use has shown that clonazepam is by far the best agent for the treatment of RBD," said Boeve. "It almost always works, even at very low doses such as 0.25 mg or 0.5 mg. Even a dosage as high as 1 mg per night is effective in almost 90% of patients. No one really understands why clonazepam works so well. It not only suppresses the vivid acting out while dreaming, but also helps to quell other bothersome nocturnal manifestations, such as the nasty nightmares that appear to reflect chasing and attacking themes."

Boeve added that, in his experience, melatonin is also useful by itself or in combination with clonazepam. Although it is not as effective as clonazepam, he said that he gives a trial of melatonin to patients with dementia before trying clonazepam because clonazepam has been associated with adverse effects on cognition. "[Dosages of] melatonin between 3 mg and 12 mg per night works at least half of the time," he said.

"We also have had some success with ramelteon [Rozerem], which is a new melatonin receptor agonist, and it seems to be effective especially in refractory cases," Boeve continued. Alternative treatments recommended by Boeve include quetiapine (Seroquel) and sodium oxybate (Xyrem), although he cautioned that impaired cognition is an adverse effect of the latter. "Overall, I would rank clonazepam as number 1 in treating RBD and melatonin as number 2, followed by a smattering of other medications that can be tried on an individual patient basis," he concluded.

http://www.appneurology.com/showArticle.jhtml?articleId=193104734

NO HYPE
07-04-2007, 05:53 AM
22 May 2007

The creatine transporter: Molecular properties and importance for cellular energy metabolism

Creatine and phosphocreatine play a key role in both ATP buffering, and high energy phosphate shuttling, in cells with high energy demands. Creatine is obtained from endogenous synthesis or from the diet. Creatine supplements are widely used to enhance muscle performance. However, we now appreciate that creatine also plays a critical role in brain function. It is neuroprotective in many animal models of neurological diseases and human trials are testing whether creatine can be used to treat Parkinson?s and Huntington?s disease. Our research concerns a specific membrane protein, the creatine transporter, required for the cellular uptake of creatine. This transporter is a member of the family of sodium- and chloride dependent neurotransmitter transporters. Mutations in the creatine transporter gene result in a novel form of X-linked mental retardation associated with a complete absence of creatine in the brain.We want to understand the importance of the creatine transporter for brain function. Antibodies against the creatine transporter are used to identify cells that are able to take up creatine. The activity and regulation of the creatine transporter are studied in cell culture models. Biochemical and molecular biology techniques have been used to investigate the mechanism of creatine transport and understand the specificity of substrate binding.

http://www.auckland.ac.nz/uoa/about/events/2007/05/seminars/energy2.cfm

NO HYPE
07-04-2007, 06:31 AM
To anyone with a REM sleep behavior disorder, please pay close attention to this article and get yourself some melatonin. I can honestly tell you that this sleep disorder was a prominent issue for many years prior to my father developing dementia.... If only I had known!


So aside from REM sleep disorders, it appears that loss of smell is yet another early indicator of neurological disease. Ironically, my father had no sense of smell for the majority of his life.



Alpha-synuclein pathology in the olfactory pathways of dementia patients

Lewy-type pathology is a characteristic of a number of neurodegenerative disorders, including Parkinson's disease and dementia with Lewy bodies. Thus far, the definitive diagnosis of these dementias can only be confirmed at post-mortem. However, it is known that the loss of smell (anosmia) is an early symptom in patients who develop dementia, and the use of the smell test has been proposed as an early diagnostic procedure The aim of this study was to understand further the extent of Lewy pathology in the olfactory system of patients with neurodegenerative disorders. Post-mortem tissue from 250 subjects was obtained from the OPTIMA brain bank. Five areas of the olfactory pathway were examined by immunolabelling for alpha-synuclein ? a major component of Lewy pathology: the olfactory tract/bulb (n = 79), the anterior olfactory nucleus in the lateral olfactory gyrus (n = 193), the region of olfactory projection to the orbito-frontal cortex (n = 225), the hippocampus (n = 236) and the amygdala (n = 201). Results show that Lewy pathology affects different parts of the olfactory pathways differentially, suggesting a specific pattern of development of pathology. Clinical Parkinson's disease is most likely to be identified if the orbito-frontal cortex is affected, while the diagnosis is less likely if the pathology is restricted to the olfactory bulb or tract. These results suggest that pathology in the olfactory bulb and tract occurs prior to clinical signs of Parkinson's disease. Furthermore, the results presented here provide further evidence supporting the possible value of a smell test to aid the clinical diagnosis of neurodegenerative diseases.

http://www.blackwell-synergy.com/doi/abs/10.1111/j.1469-7580.2007.00748.x

NO HYPE
01-09-2008, 03:30 PM
Expert Rev Neurother. 2008 Jan;8(1):133-58.

Lifestyle-related factors in predementia and dementia syndromes.

Cognitive decline and dementia have a deep impact on the health and quality of life of older subjects and their caregivers. Since the therapeutic options currently available have demonstrated limited efficacy, the search for preventive strategies for cognitive decline and dementia are mandatory. A possible role of lifestyle-related factors was recently proposed for age-related changes of cognitive function, predementia syndromes and the cognitive decline of degenerative (Alzheimer's disease [AD]) or vascular origin. At present, cumulative evidence suggests that vascular risk factors may be important in the development of mild cognitive impairment (MCI), dementia and AD. Moderate alcohol drinking has been proposed as a protective factor against MCI and dementia in several longitudinal studies, but contrasting findings also exist. The Mediterranean diet could therefore be an interesting model with which to further study the association between dietary patterns and cognitive functioning, given the suggested role of many components of this diet (monounsaturated fatty acids, polyunsaturated fatty acids, cereals and red wine) in contrasting cognitive impairment and dementia. The association between low education and predementia and dementia syndromes is supported by the majority of studies, but very few studies have investigated whether this association may be attributed with lifestyle factors that covary with education. Studies in the literature seem to identify in physical exercise one promising strategy in decreasing cognitive decline, but some of the limitations of these studies do not allow us to draw definite conclusions. At present, in older subjects, healthy diets, antioxidant supplements, the prevention of nutritional deficiencies, and moderate physical activity could be considered the first line of defense against the development and progression of predementia and dementia syndromes. However, in most cases, these were only observational studies, and results are awaited from large multicenter randomized clinical trials in older persons that may clarify the possible synergy, for example, between moderate exercise, physical activity and healthy Mediterranean diet on cognition in the elderly.

swarfmaker
02-28-2008, 03:38 PM
How has you father been doing on your anti-oxidant protocol?

Peter LeDrew
02-28-2008, 05:42 PM
Kudos to the staff at AOR providing the latest news in supplementation and health!
http://www.aor.ca/int/news.php


Effectiveness of Citi****ne Supplementation Demonstrated in Detail by New Technology



Citi****ne belongs to a category of supplements whose potency and benefits far exceed any degree of public awareness they have been able to generate, even among medical practitioners and preventative health professionals alike. This is an ironic phenomenon, curious but by no means rare and certainly not limited to the world of natural health. However, a new study utilizing cutting-edge medical technology might create some new converts to the potential of citi****ne supplementation while further cementing the belief of the faithful.

Citi****ne supplementation has been used as a potential treatment for ischemic stroke, traumatic brain injury, memory impairment and various other cognitive conditions, as well as amblyopia and even glaucoma. Magnetic resonance spectroscopy (MRS) studies have previously demonstrated that oral citi****ne supplementation alters phosphorus metabolites in brain. This is significant because phosphorous is highly ubiquitous and essential for energy production. The vitamin B complex, itself critical to energy and neurological function, relies heavily on phosphorus, which also forms an integral part of both ATP (the universal source of all cellular energy) and its precursor, phosphocreatine.

The new technology used a three-dimensional chemical-shift imaging (3D-CSI) protocol on sixteen healthy men and women who orally self-administered 500mg or 2000mg of citi****ne for six weeks. The results of this study, conducted at the Cognitive Neuroimaging Laboratory and Brain Imaging Center at McLean Hospital in Belmont, MA, revealed that citi****ne supplementation (at both doses) significantly increased levels of phosphocreatine and beta NTP, primary indicators of high energy phosphate and ATP levels respectively. Furthermore, these increases were found exclusively in the anterior cingulate cortex, which is a fibrous bundle responsible for relaying neural signals between the left and right sides of the brain. This sheds further light on citi****ne?s mechanism of action, demonstrating that its effects are not simply health-enhancing on a general antioxidant or nutrient support level, but also unambiguous and definitive with respect to positively altering distinct neurological markers in a specific part of the brain.

Obtained from: Silveri et al. Oral Citi****ne supplementation significantly alters phosphorus metabolites in the anterior cingulate cortex. Journal of NeuroScience, Published Ahead of Print, March 2008.

NO HYPE
02-28-2008, 07:01 PM
I can have our M.D. forward me his protocol for dementia if you're interested.

Re-repped.:)

NO HYPE
02-28-2008, 07:53 PM
How has you father been doing on your anti-oxidant protocol?

In terms of limiting disease progression, he is doing rather well. However, he is currently having some circulatory problems (i.e. blood-pooling in the feet/sometimes hands). It's difficult with DLB, as the individual's posture is often significantly affected, thereby limiting the amount of achievable exercise. I have definitely noticed that the overwhelming amount of oxidative damage occurs at the end of the day, and this is reflective of his symptoms. This is the reason I am now thinking of dividing the protocol into 2 categories (i.e. supplements for glutathione enhancement and supplements for BBB permeation).

I'm thinking of administering the glutathione-targeted orals in the AM, and the BBB-targeted orals in the evening (to compensate for the up-regulated oxidation/neuronal degeneration).

NO HYPE
02-29-2008, 04:27 AM
With the exception of alpha-synuclein accumulation and somatic dysfunction, inflammation and oxidation are the key physiological substrates underlying the progression of dementia.


Expert Rev Neurother. 2008 Jan;8(1):133-58.

Lifestyle-related factors in predementia and dementia syndromes.

Cognitive decline and dementia have a deep impact on the health and quality of life of older subjects and their caregivers. Since the therapeutic options currently available have demonstrated limited efficacy, the search for preventive strategies for cognitive decline and dementia are mandatory. A possible role of lifestyle-related factors was recently proposed for age-related changes of cognitive function, predementia syndromes and the cognitive decline of degenerative (Alzheimer's disease [AD]) or vascular origin. At present, cumulative evidence suggests that vascular risk factors may be important in the development of mild cognitive impairment (MCI), dementia and AD. Moderate alcohol drinking has been proposed as a protective factor against MCI and dementia in several longitudinal studies, but contrasting findings also exist. The Mediterranean diet could therefore be an interesting model with which to further study the association between dietary patterns and cognitive functioning, given the suggested role of many components of this diet (monounsaturated fatty acids, polyunsaturated fatty acids, cereals and red wine) in contrasting cognitive impairment and dementia. The association between low education and predementia and dementia syndromes is supported by the majority of studies, but very few studies have investigated whether this association may be attributed with lifestyle factors that covary with education. Studies in the literature seem to identify in physical exercise one promising strategy in decreasing cognitive decline, but some of the limitations of these studies do not allow us to draw definite conclusions. At present, in older subjects, healthy diets, antioxidant supplements, the prevention of nutritional deficiencies, and moderate physical activity could be considered the first line of defense against the development and progression of predementia and dementia syndromes. However, in most cases, these were only observational studies, and results are awaited from large multicenter randomized clinical trials in older persons that may clarify the possible synergy, for example, between moderate exercise, physical activity and healthy Mediterranean diet on cognition in the elderly.

DRP7
02-29-2008, 04:30 AM
last year there was a seminal study that showed a large positive effect from mediterranean type diet style on dementia risk.

NO HYPE
02-29-2008, 05:18 AM
last year there was a seminal study that showed a large positive effect from mediterranean type diet style on dementia risk.

Good to know.

I have recently viewed some rather positive results in the downregulation of degenerative decline/neuronal apoptosis, via the administration of TUDCA (i.e. Bile acids and apoptosis modulation: an emerging role in experimental Alzheimer's disease). It looks like LiverLonger may aquire some benefits that we were not aware of. :)

shefler29
03-01-2008, 01:20 PM
Just to add I saw a study that at least 800mcg of folic acid also help with preventing dementia.

http://news.yahoo.com/s/afp/20080205/hl_afp/healthageingdementia

hope this helps

Orange Triad and NOW ADAM both contain 800mcg fyi

swarfmaker
03-01-2008, 08:27 PM
I'm glad that you have been having success, even if only in part. My mother was diagnosed late last year with another type of neuro-degenrative disease called corticobasal degeneration (CBD or cortical basal ganglionic degeneration, CBGD). It seems that these illnesses all share some common causes, and my just be different manifestations of similar processes.

I've gone through the posts in this thread and come up with a long list of supplements that might be effective. Wow.

As I understand it, you are giving your father the following:

2 capsules of huperzine 2x a day
1 capsule of picamilon/choline 2x a day

Also mentioned in the various posts, but without how much and how often are:

N-Acetyl-Cysteine [NAC]
ALA
ubiquinol/idebenone
curcumin
selenium
fish oil
vitamin C
vitamin A
vitamin E
melatonin
silymarin
picamilon
CDC choline
5-HTP
EPA/DHA
sesamin
5-Loxin
carnosine
Methyl B-12
Pyritinol
vincamine
Hydergine
Geen tea
resveratrol
gingko biloba
piracetam [available in Greece?]
Coenzyme Q10
creatine
Citi****ne
TUDCA
folic acid (vitamin B-9; 800mcg)
CM

Are you giving your father some of these too?

How much and how often?

Some other notes I found...

"Note: avoid administering vitamin C and NAC simultaneously during inflammatory response as it may promote hydroxyl radical formation in the presence of iron (Fe2+)."

Antioxidants to assist in inhibiting excessive cytochrome P450-induced, free radical cell damage: NAC, silymarin, ALA

Nootropics: huperzine A, picamilon, and CDC choline (as well as 5-HTP)

L-Huperzine A: 400 mcg (micro grams), given no other potent ACh compound is given.

What are the "other potent ACH" compounds?

For inflammation (targeting COX, NF-κB , LOX pathways ): EPA/DHA, sesamin, curcumin, and 5-Loxin

"...considering the inclusion of CM (along with creatine) to this protocol"

"...TUDCA (for downregulation of degenerative decline/neuronal apoptosis "Bile acids and
apoptosis modulation: an emerging role in experimental Alzheimer's disease")"

Also "I'm thinking of administering the glutathione-targeted orals in the AM, and the BBB-targeted orals in the evening (to compensate for the up-regulated oxidation/neuronal degeneration)"

Which supplements target glutathione?

What are "polyphenol antioxidants"?


In terms of limiting disease progression, he is doing rather well. However, he is currently having some circulatory problems (i.e. blood-pooling in the feet/sometimes hands). It's difficult with DLB, as the individual's posture is often significantly affected, thereby limiting the amount of achievable exercise. I have definitely noticed that the overwhelming amount of oxidative damage occurs at the end of the day, and this is reflective of his symptoms. This is the reason I am now thinking of dividing the protocol into 2 categories (i.e. supplements for glutathione enhancement and supplements for BBB permeation).

I'm thinking of administering the glutathione-targeted orals in the AM, and the BBB-targeted orals in the evening (to compensate for the up-regulated oxidation/neuronal degeneration).

NO HYPE
03-02-2008, 08:59 AM
Current protocol consists of:

TUDCA
NAC
Na-R-ALA
resveratrol
grape seed extract
gingko biloba
vitamin C
silymarin
curcumin
CDC choline
EPA/DHA
Coenzyme Q10
melatonin
B-complex
Methyl B-12
folic acid


Supplements that I would like to add:

Pyritinol
vincamine
Hydergine
Scyllitol

Note: considering EDTA for iron chelation

NO HYPE
03-02-2008, 09:00 AM
I'm thinking of administering the glutathione-targeted orals in the AM, and the BBB-targeted orals in the evening (to compensate for the up-regulated oxidation/neuronal degeneration)


Which supplements target glutathione?

NAC, Na-R-ALA, SAMe, silymarin, ect.




What are "polyphenol antioxidants"?

Resveratrol, grape seed extract, ect. http://en.wikipedia.org/wiki/Polyphenol_antioxidant

NO HYPE
03-02-2008, 09:32 AM
My mother was diagnosed late last year with another type of neuro-degenrative disease called corticobasal degeneration (CBD or cortical basal ganglionic degeneration, CBGD).

Yes. I remember your PM.


I would be more than happy to share my information however, I will need to first, do a little research on the pathology of cellular degeneration that accompanies this disease.

Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia. Corticobasal degeneration progresses gradually. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body (unilateral), but eventually affect both sides as the disease progresses. Symptoms are similar to those found in Parkinson disease, such as poor coordination, akinesia (an absence of movements), rigidity (a resistance to imposed movement), disequilibrium (impaired balance); and limb dystonia (abnormal muscle postures). Other symptoms such as cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing) may also occur. An individual with corticobasal degeneration eventually becomes unable to walk.

Corticobasal degeneration usually progresses slowly over the course of 6 to 8 years. Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism.
http://www.ninds.nih.gov/disorders/corticobasal_degeneration/corticobasal_degeneration.htm

More info: http://memory.ucsf.edu/Education/Disease/cbd.html




It seems that these illnesses all share some common causes, and my just be different manifestations of similar processes.

The neuroinflammation/degeneration that occurs in these disorders, is often accompanied by significantly increased levels of circulating peripheral TNF-alpha and/or ROS-induced oxidative damage. This is the reason why supplemented antioxidants are so vital in the suppression of neurodegenerative decline.

NO HYPE
03-02-2008, 09:37 AM
EXCERPTS FROM:
Toxicological Sciences 2005 84(1):139-148; doi:10.1093/toxsci/kfi055
Manganese Potentiates In Vitro Production of Proinflammatory Cytokines and Nitric Oxide by Microglia Through a Nuclear Factor kappa B?Dependent Mechanism

Recent evidence suggests that the mechanism of manganese (Mn) neurotoxicity involves activation of microglia and/or astrocytes; as a consequence, neurons adjacent to the activated microglia may be injured.

Mn moderately increased interleukin-6 and tumor necrosis factor alpha (TNF-a) production only at higher Mn concentrations, which were cytotoxic. At all LPS doses, however, proinflammatory cytokine production was dose-dependently increased by Mn. Similarly, LPS-induced NO production and iNOS expression were substantially enhanced by Mn. Pharmacological manipulations indicated that nuclear factor kappa B (NFB) activation is critical for the observed enhancement of cytokine and NO production. Within the context of inflammation, increased production of proinflammatory cytokines and NO by Mn could be an important part of the mechanism by which Mn exerts its neurotoxicity.

the neurotoxic effects of Mn have traditionally been associated with direct effects of this metal on neuronal cells, with selective accumulation within the basal ganglia, induction of mitochondrial dysfunction, and induction of neurotransmitter imbalance contributing to the neurotoxicity of Mn (e.g., Aschner, 2000; Aschner and Aschner, 1991; Verity, 1999). However, the present studies suggest an additional mechanism, which might be particularly important within the context of ongoing inflammation--namely, a possible contribution to the neurotoxicity of Mn by inflammatory products from microglia.

Although the exact mechanisms of Mn neurotoxicity are still being unraveled, the neurotoxic effects of Mn have traditionally been associated with direct effects of this metal on neuronal cells, with selective accumulation within the basal ganglia, induction of mitochondrial dysfunction, and induction of neurotransmitter imbalance contributing to the neurotoxicity of Mn (e.g., Aschner, 2000; Aschner and Aschner, 1991; Verity, 1999). However, the present studies suggest an additional mechanism, which might be particularly important within the context of ongoing inflammation?namely, a possible contribution to the neurotoxicity of Mn by inflammatory products from microglia.

The current results clearly demonstrate that Mn enhances TNF-, IL-6, and NO production by LPS-activated microglia, and that this enhancement is NFB-dependent. The increased iNOS expression and subsequent NO production confirm the Mn effects reported elsewhere (Chang and Liu, 1999). However, the proinflammatory cytokine increases and the overall dependency of the cytokine and NO increases caused by Mn on NFB activation have not been reported previously. In the absence of LPS, Mn was not capable of stimulating microglial NO production (our results, as well as those of Chang and Liu [1999]); Mn also induced minimal cytokine production. However, in the presence of LPS, cytokine production was markedly enhanced by Mn (either as MnCl2 or as MnSO4). This indicates that, for Mn to exert its potentiating effects, the presence of an inflammogen, such as LPS, is necessary.

Elevated proinflammatory cytokine expression in the brain has been found in post mortem examination of brains of PD patients, as well as in animal models of PD (Nagatsu et al., 2000; Sriram et al., 2002). Moreover, pharmacological inhibition of TNF- synthesis, or deletion of TNF- (Ferger et al., 2004) or its receptors (Sriram et al., 2002), attenuates the basal ganglia toxicity of MPTP in mice.

In addition to proinflammatory cytokines, an increase in NO, via increased expression of iNOS, has been associated with PD-like pathology (Tieu et al., 2003). For example, mice deficient in iNOS were protected from MPTP toxicity, which suggests that reactive nitrogen intermediates, such as NO and its toxic metabolite peroxynitrite (ONOO?), contribute to dopaminergic neuronal cell death, possibly by inhibiting components of the mitochondrial respiratory chain and, as a result, they compromise the energy state of the cells (Heales et al., 1999). Even more interesting is the fact that neurons, in contrast to other resident cells, such as astrocytes and microglia, are susceptible to NO and ONOO? exposure, whereas the principal producers of NO/ONOO? in the brain, the microglia and the astrocytes, are relatively resistant (Heales et al., 1999). Moreover, dopaminergic neurons are twice as sensitive to LPS toxicity as neurons that are negative for tyrosine hydroxylase (TH, the rate limiting-enzyme for dopamine synthesis, Bronstein et al., 1995). Considering the fact that cytokines, like TNF-, can be directly cytotoxic to neurons (Sipe et al., 1996) and can (either by themselves or in combination with LPS) enhance NO-dependent cytotoxicity, e.g., in PC12 cells (Heneka et al., 1998), the importance of increased proinflammatory cytokine generation in PD patients (Nagatsu et al., 2000) and in the MPTP model of PD (Sriram et al., 2002) becomes apparent. Of particular interest is the finding that maneb enhanced the neuronal damage caused by MPTP, the basal ganglia effects of which are dependent on microglial activation (Takahashi et al., 1989).

NO HYPE
03-02-2008, 09:38 AM
The present results suggest that microglia-derived proinflammatory cytokines and NO might play a major role in Mn neurotoxicity when microglia are also exposed to an inflammagen. This finding does not appear to be unique to Mn as, for example, the basal ganglia toxicity of MPTP was substantially enhanced by LPS (Gao et al., 2003). However, MPTP is a model toxicant, and the likelihood for exposure to it, other than accidentally, is minimal. Mn, on the other hand, is both occupationally and environmentally relevant (Aschner, 2000). Similarly, LPS, a component of the Gram-negative bacterial cell, is widely distributed in the environment, including in house dust (Michel et al., 1996) and various agricultural settings (Kullman et al., 1998). Importantly, systemic inflammation activates brain microglia and has been associated with neurodegeneration (Perry et al. 2003). Moreover, proinflammatory cytokines and bacterial products, such as LPS, readily cross the blood?brain barrier (Banks et al. 2002). Thus, the possibility of Mn and LPS interacting within the brain and stimulating microglial production of inflammatory mediators is distinct in cases where the opportunity for co-exposure exists. For example, many agricultural workers are exposed to other hazardous chemicals, such as pesticides, in conjunction with LPS, and some of these pesticides, such as maneb, contain Mn, which has already been reported to synergistically increase the dopaminergic toxicity of paraquat (Thiruchelvam et al., 2003; Takahashi et al., 1989). Even more intriguing, however, is recent evidence suggesting that pretreatment with Mn increased the susceptibility of mice to a subsequent viral infection (viruses that infect the brain), and that the increased susceptibility was manifested with brain inflammation of earlier onset and greater magnitude than that observed in control, non-Mn-treated mice (Seth et al., 2003).

Although the results of the present study and those of Chang and Liu (1999) have implicated microglia as important players in Mn-induced neurotoxicity, especially in the presence of an inflammogen (Spranger et al., 1998), and, very recently (Barhoumi et al., 2004) have demonstrated that astrocytes exposed to Mn combined with the cytokines IL-1b and IFN- (Spranger et al., 1998), or with LPS (Barhoumi et al., 2004) have iNOS-derived enhanced production of NO. These reports demonstrate that the effects of combined Mn plus inflammagen exposure on iNOS/NO do not appear to be specific only to microglia. More importantly, however, these reports raise the question of the importance of astrocytes relative to microglia in Mn neurotoxicity, within the context of an inflammatory stimulus. Even though astrocytes outnumber microglia in the brain, it has been demonstrated that microglia are non-uniformly distributed in the brain (the substantia nigra, basal ganglia, hippocampus have the greatest numbers; Lawson et al., 1990), and that addition of microglia to mixed glial?neuronal cultures from brain regions with low microglial numbers such as the cortex, renders these cultures as sensitive to the effects of LPS, as are mixed striatal cultures (Kim et al., 2000). Moreover, in vivo, as well as in mixed microglia-astrocyte cultures, increased NO and iNOS expression after LPS + IFN- stimulation is exclusively microglia-derived (Possel et al., 2000). Also, microglia, but not astrocytes, possess NADPH oxidase, which allows them to generate superoxide free radical, and, ultimately peroxynitrite (Gao et al., 2003). In addition, LPS alone was capable of inducing proinflammatory cytokine expression, including that of cell-associated IL-1b, in highly purified cultures of microglia, whereas LPS failed to stimulate cytokine expression by astrocytes. On the other hand, IL-1b was a strong stimulus for astrocytes, suggesting that microglia are key regulators of astrocyte response, perhaps working primarily through the expression of cell-associated IL-1b (Lee et al., 1993). Interestingly, the studies of Spranger et al. (1998), which suggested that astrocytes are more sensitive to Mn than are microglia, used the IFN- + IL-1b combination as the additional stimulus for iNOS expression. Overall, these findings, combined with the facts that activated microglia are readily detected in striatum and substantia nigra of PD patients and in MPTP-treated mice (Olanow and Tatton, 1999; Czlonkowska et al., 1996) and more importantly, that microglial activation preceded astrocytosis in the MPTP model of PD (Kohutnicka et al., 1998), suggest that microglia are important contributors to dopaminergic neurotoxicity. Their importance arises from their differential distribution, reactivity to stimuli, ability to stimulate astrocytes, and relative insensitivity to potential toxic products that they produce.

So far, all of the studies evaluating the potential of Mn as a modulator of inflammatory mediators, including our study, have been conducted in vitro. Although they all demonstrate the ability of Mn to enhance proinflammatory cytokine and/or NO production by either microglia or astrocytes, only future in vitro studies with mixed cultures and, ultimately, in vivo experiments will (1) confirm these findings and (2) decipher the relative importance of microglia and astrocytes in Mn-induced neurodegeneration with and without ongoing inflammation. It must not be overlooked in such studies that neuronal cells themselves are capable of producing NO (derived from neuronal NOS) when stimulated with cytokines and/or LPS (e.g., Heneka et al., 1998). Moreover, the role of reactive substances that are released from damaged neurons and are capable of activating microglia should be taken into account. In light of the known neuronal mitochondrial dysfunction caused by Mn exposure (Aschner, 2000), the ability of signals from Mn-damaged neurons to enhance the direct effect of this metal on microglial activation, even in the absence of an inflammagen, needs to be considered.

Our pharmacological experiments suggest that both increased cytokine production and iNOS expression are NFB-dependent. The exact mechanism of the NFB activation by the Mn-LPS combination is unknown at present. One possibility, however, is an alteration of iron homeostasis by Mn. In this regard, Zheng and Zhao (2001) reported that Mn exposure increased cellular iron uptake in PC12 cells, but not in astrocytes. Moreover, iron plays a major role in NFB activation and subsequent proinflammatory cytokine production by inflammation activated peripheral macrophages (Xiong et al., 2004). The transcriptional regulatory factor NFB binds to elements present in the promoter regions of many of the proinflammatory cytokines, TNF- and IL-6 included, as well as to the promoter of iNOS (Abraham, 2000; Aktan, 2004). As a result of increased activation of NFB, the expression of these proinflammatory cytokines and the iNOS-dependent production of NO are enhanced. It has been suggested that NFB activation is a central event in the development of acute inflammatory injury associated with critical illness (Abraham, 2000). Additionally, a central role of NFB activation and ensuing transactivation of promoters of inflammatory cytokines in neurodegenerative processes, such as PD, has been suggested (Youdim et al., 1999).

Although inhibition of NFB was highly effective in preventing the enhancing effects of Mn on TNF-, IL-6 and iNOS, addition of either of the antioxidants Trolox or NAC was only marginally effective. Somewhat in contrast, Barhoumi et al. (2004) reported that in C6 gliomas, addition of the mitochondrion-specific antioxidant MitoQ diminished the enhancement of iNOS caused by the Mn plus LPS combination. It should be noted however, that (1) the cell line used by these investigators is of astrocytic origin and, thus, possibly accumulated more Mn; (2) Trolox and NAC are not mitochondrion-specific; and (3) iNOS enhancement was diminished, but not eliminated, by MitoQ. In this regard, the central role of increased oxidative stress within the cell on subsequent NFB activation, even though demonstrated in various experimental paradigms, has been recently questioned. At best, the evidence for the involvement of oxidative stress is inconclusive; such stress may be only facilitative (Bowie and O'Neill, 2000) or nonexistent, as it was for TNF- mRNA induction by LPS (White and Tsan, 2001). The differential effects of NAC and Trolox on TNF- and IL-6 production by microglia seen in the present experiments have been observed in other experimental paradigms. For example, in vivo pretreatment of mice challenged with LPS with NAC, diminished the subsequent induction of serum TNF-a, but not that of IL-6 (Peristeris et al., 1992). Moreover, the activation of the transcription factor AP-1, but not the activation of NFB, was inhibited by Trolox pretreatment (Rensing et al., 2001), raising the possibility that AP-1 plays a greater role in IL-6 induction in microglia than it does in TNF- induction in the absence of Mn.

Lipopolysaccharides and other inflammatory stimuli activate numerous intracellular signaling pathways, many of which converge on NFB and, ultimately, lead to increased cytokine production. Thus, LPS activates several mitogen-activated protein (MAP) kinases, including the extracellular signal-regulated kinase (ERK), the stress-activated protein kinases (SAPK), and the p38 kinase. Often these kinases function in a cooperative manner (Zhu et al., 2000), but addition of a p38 inhibitor to LPS-stimulated macrophages blocks LPS-stimulated TNF- production, thus suggesting a critical role for the p38 kinase (Kraatz et al., 1999). Although the exact mechanism of the Mn-induced enhancement of NFB activation is unknown at present, preliminary evidence indicates that p38 kinase is involved (Crittenden and Filipov, 2004).

In summary, microglia exposed to Mn, in combination with an inflammagen, respond with enhanced production of proinflammatory cytokines and NO. Thus, the role of brain microglia in the mechanisms of Mn neurotoxicity, especially within the context of inflammation, should not be overlooked.

http://toxsci.oxfordjournals.org/cgi/content/full/84/1/139
http://toxsci.oxfordjournals.org/cgi/reprint/84/1/139.pdf

NO HYPE
03-02-2008, 09:43 AM
one important fact to consider, is the excessive iron accumulation that has been shown to contribute to the etiology of neurodegenerative disorders.

Ageing Research Reviews. Volume 3, Issue 3, July 2004, Pages 327-343
Does cellular iron dysregulation play a causative role in Parkinson?s disease?

Selective dopaminergic cell loss in Parkinson?s disease is correlated with increased levels of cellular iron. It is still hotly debated as to whether the increase in iron is an upstream event which acts to promote neurodegeneration via formation of oxidative stress or whether iron accumulates as a by-product of the neuronal cell loss. Here we review evidence for loss of iron homeostasis as a causative factor in disease-associated neurodegeneration and the primary players which may be involved. A series of recent studies suggest that iron regulatory proteins (IRPs) coordinate both cellular iron levels and energy metabolism, both of which are disrupted in Parkinson?s disease (PD) and may in turn contribute to increased levels of oxidative stress associated with the disease. Iron has also been recently been implicated in promotion of α-synuclein aggregation either directly or via increasing levels of oxidative stress suggesting an important role for it in Lewy body formation, another important hallmark of the disease. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6X1H-4CJV7TB-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0c436894c8df1c3006f6626d9926b597



EXERPTS FROM:
Molecular Interventions 6:89-97, (2006)
American Society for Pharmacology and Experimental Therapeutics 10.1124/mi.6.2.6
Iron Dysregulation and Neurodegeneration: The Molecular Connection

Iron is essential for many biological processes however excess concentrations can be harmful to many tissues. Its amounts must therefore be carefully regulated in all cells of the body including those in the brain. Increased amounts of iron have been reported in many neurodegenerative disorders. Whether this increased iron contributes to neurodegeneration has been considered controversial. In this review, we discuss some recently identified anomalies in proteins linked with iron metabolism which signify a critical role for iron dysregulation in neurodegeneration.

The management of iron is a critical issue for all living cells, where its presence is necessary for carrying out numerous vital biological reactions, but because of its highly reactive nature, iron is extremely toxic if its concentrations are not tightly regulated intracellularly. The divalent state of iron makes it highly toxic, as it can rapidly react with hydrogen peroxide and molecular oxygen to produce free radicals. Free radical formation can promote lipid peroxidation, DNA strand breaks, and modification or degradation of biomolecules, eventually leading to cell death. Cells have therefore evolved a sophisticated mechanism consisting of an array of proteins that regulate the amount of free iron in cells by modulating its uptake, storage, and export. Together, these proteins provide a state of cellular equilibrium whereby iron is readily available for all metabolic functions but sheltered from taking part in cytotoxic reactive oxygen species (ROS)-generating reactions (1, 2).

Iron plays crucial role in the brain where it is required to sustain the brain?s high respiratory activity, for myelinogenesis, and for the production of several neurotransmitters such as dopamine, norepinephrine, serotonin, and generation of -aminobutyric acid (GABA)ergic activity (3). In spite of its requirement, high levels of iron are of particular concern for the brain because of iron?s intense oxidative metabolism, which generates large amounts of ROS. In addition, the toxic effects of iron on brain cells are more pronounced because of their limited regenerative capabilities. It is therefore fortunate that iron must cross an additional obstacle in the form of the blood-brain-barrier to enter brain cells. The exact mechanism of iron uptake and export from the brain is not fully understood. Most of the proteins involved in the maintenance of iron metabolism are expressed in the brain, suggesting that brain cells follow similar homeostatic mechanisms as do all other cells in the body (4). It is also known that the brain accumulates iron in normal aging, which suggests that there is more import of iron into the brain than export. These increased levels of iron could place the brain iron homeostatic mechanism under pressure and make it more likely to err. Abnormal amounts of iron in the brain have been demonstrated in a number of age-related neurodegenerative disorders including Alzheimer Disease (AD) (5) and Parkinson Disease (PD) (6). Although it is generally acknowledged that this excess iron catalyzes the formation of ROS and induces oxidative damage to which the brain is particularly sensitive, brain iron accumulation itself has not, until recently, been widely considered a primary cause of neurodegeneration.

With the discovery of other proteins (such as DMT1, ceruloplasmin, ferroportin, hephaestin, etc.), a more detailed picture of iron maintenance is beginning to be better appreciated, including the realization that there are likely more molecules involved in iron regulation that have yet to be identified . This is especially true for brain iron metabolism, which requires additional mechanisms that regulate the connection between systemic iron circulation and passage through the blood-brain-barrier to sustain the brain?s need for iron.

The identification of the mutations described above establish that mutations that specifically effect iron metabolism have the ability to affect the brain and cause neurodegeneration. This conclusion implies that iron overload in the brain??seen in many neurodegenerative disorders??could be causative and not just an inconsequential outcome. More research is needed to fully understand brain iron metabolism and the molecular mechanisms that cause specific brain areas to accumulate iron in different diseases. Of equal importance is the need to develop appropriate iron chelators whose effects, when properly titrated, effectively reduce iron concentrations in the brain but do not shift the brain towards undesirable iron deficiency. Currently, the metal chelator, clioquinol (64) and VK28 series of iron chelators (65) are being investigated for AD and PD, respectively. http://molinterv.aspetjournals.org/cgi/content/full/6/2/89



1: Mov Disord. 2006 Sep;21(9):1299-310. Links
Iron metabolism in Parkinsonian syndromes.

Growing evidence suggests an involvement of iron in the pathophysiology of neurodegenerative diseases. Several of the diseases are associated with parkinsonian syndromes, induced by degeneration of basal ganglia regions that contain the highest amount of iron within the brain. The group of neurodegenerative disorders associated with parkinsonian syndromes with increased brain iron content can be devided into two groups: (1) parkinsonian syndromes associated with brain iron accumulation, including Parkinson's disease, diffuse Lewy body disease, parkinsonian type of multiple system atrophy, progressive supranuclear palsy, corticobasal ganglionic degeneration, and Westphal variant of Huntington's disease; and (2) monogenetically caused disturbances of brain iron metabolism associated with parkinsonian syndromes, including aceruloplasminemia, hereditary ferritinopathies affecting the basal ganglia, and panthotenate kinase associated neurodegeneration type 2. Although it is still a matter of debate whether iron accumulation is a primary cause or secondary event in the first group, there is no doubt that iron-induced oxidative stress contributes to neurodegeneration. Parallels concerning pathophysiological as well as clinical aspects can be drawn between disorders of both groups. Results from animal models and reduction of iron overload combined with at least partial relief of symptoms by application of iron chelators in patients of the second group give hope that targeting the iron overload might be one possibility to slow down the neurodegenerative cascade also in the first group of inevitably progressive neurodegenerative disorders. (c) 2006 Movement Disorder Society. http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=16817199&cmd



1: Top Magn Reson Imaging. 2006 Feb;17(1):5-17. Links
Role of iron in neurodegenerative disorders.

Although the pathophysiology underlying a number of neurodegenerative diseases is complex and, in many aspects, only partly understood, increased iron levels in pathologically relevant brain areas and iron-mediated oxidative stress seem to play a central role in many of them. Much has been learned from monogenetically caused disturbances of brain iron metabolism including pantothenate kinase-associated neurodegeneration type 2, hereditary ferritinopathies affecting the basal ganglia, and aceruloplasminemia that may well be applied to the most common neurodegenerative disorders associated with brain iron accumulation including Parkinson disease and Alzheimer disease. Iron-mediated oxidative stress in neurodegenerative diseases caused by other genetic pathways like Huntington disease and Friedreich ataxia underscore the complex interaction of this trace metal and genetic variations. Therapeutical strategies derived from application of iron chelators in monogenetically caused disturbances of brain iron metabolism and new iron and oxidative stress diminishing substances in animal models of Parkinson disease are promising and warrant further investigational effort. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17179893&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus



1: Mov Disord. 2007 Nov 15;22(15):2141-8.
Levodopa responsiveness in disorders with parkinsonism: A review of the literature.

A literature review was conducted to investigate whether or not levodopa (LD) responsiveness (LR) is a useful criterion in the diagnosis of parkinsonian disorders. Although LR does appear to differ among the parkinsonian disorders, there is considerable confusion in the literature. While most patients with Parkinson's disease (PD) have a sustained benefit from LD, a small minority of patients with documented PD do not respond. The literature suggests that the LR rate is higher for multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) than based on published diagnostic criteria. Magnitude and duration of response to LD and tolerability (time course, type and distribution of dyskinesias, mental effects and motor worsening) may be useful features in distinguishing PD, MSA, PSP, and CBD. Efforts should be directed toward better defining LR when used for diagnostic purposes and in scientific publications. (c) 2007 Movement Disorder Society. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17534959&ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum

NO HYPE
03-02-2008, 10:16 AM
Kudos to the staff at AOR providing the latest news in supplementation and health!
http://www.aor.ca/int/news.php


Effectiveness of Citi****ne Supplementation Demonstrated in Detail by New Technology



Citi****ne belongs to a category of supplements whose potency and benefits far exceed any degree of public awareness they have been able to generate, even among medical practitioners and preventative health professionals alike. This is an ironic phenomenon, curious but by no means rare and certainly not limited to the world of natural health. However, a new study utilizing cutting-edge medical technology might create some new converts to the potential of citi****ne supplementation while further cementing the belief of the faithful.

Citi****ne supplementation has been used as a potential treatment for ischemic stroke, traumatic brain injury, memory impairment and various other cognitive conditions, as well as amblyopia and even glaucoma. Magnetic resonance spectroscopy (MRS) studies have previously demonstrated that oral citi****ne supplementation alters phosphorus metabolites in brain. This is significant because phosphorous is highly ubiquitous and essential for energy production. The vitamin B complex, itself critical to energy and neurological function, relies heavily on phosphorus, which also forms an integral part of both ATP (the universal source of all cellular energy) and its precursor, phosphocreatine.

The new technology used a three-dimensional chemical-shift imaging (3D-CSI) protocol on sixteen healthy men and women who orally self-administered 500mg or 2000mg of citi****ne for six weeks. The results of this study, conducted at the Cognitive Neuroimaging Laboratory and Brain Imaging Center at McLean Hospital in Belmont, MA, revealed that citi****ne supplementation (at both doses) significantly increased levels of phosphocreatine and beta NTP, primary indicators of high energy phosphate and ATP levels respectively. Furthermore, these increases were found exclusively in the anterior cingulate cortex, which is a fibrous bundle responsible for relaying neural signals between the left and right sides of the brain. This sheds further light on citi****ne?s mechanism of action, demonstrating that its effects are not simply health-enhancing on a general antioxidant or nutrient support level, but also unambiguous and definitive with respect to positively altering distinct neurological markers in a specific part of the brain.

Obtained from: Silveri et al. Oral Citi****ne supplementation significantly alters phosphorus metabolites in the anterior cingulate cortex. Journal of NeuroScience, Published Ahead of Print, March 2008.

Thank you kindly for adding to the discussion Peter. CDP choline is a great supplement.

swarfmaker
03-02-2008, 03:37 PM
Have you considered IP6? I've been giving my mother about 800mg of IP6 (on an empty stomach) for about a year now. Originally we thought she had AD. But since I read the article about "Parkinsonain Syndromes" and iron metabolism ("Inhibition of iron-Iron metabolism in Parkinsonian syndromes" Mov Disord. 2006 Sep;21(9):1299-310. http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=16817199&cmd=showdetailview
However, I'm not sure how much to give her. The IP6 I buy is actually sold as an immune system booster, and for that they take it in grams!

Here's an article about IP6...
"Inhibition of iron-catalysed hydroxyl radical formation by inositol polyphosphates: a possible physiological function for myo-inositol hexakisphosphate"
Phillip T. HAWKINS, David R. POYNER,* Trevor R. JACKSON, Andrew J. LETCHER, David A. LANDER and Robin F. IRVINE Department of Biochemistry, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge CB2 4AT, U.K.

"In 1984, Graf et al. showed that InsP. was a particularly effective inhibitor of iron-catalysed hydroxyl radical (OH') formation, and suggested that it might make a useful food additive (Graf et al., 1984, 1987; Graf and Eaton, 1990)."

"Some idea of the relative affinity of InsP6 for Fe3+ was deduced by competition experiments measuring the decolorization of FeCl3/catechol complexes (see the Materials and methods section). Any compound that is able to compete with catechol for Fe3+ in the same concentration range as the Fe'+-catechol complex (0.25 mM in this case) must have an affinity for Fe3+
that is of a similar order to, or greater than, that of catechol (the K1 for which is approx. 10-20; Martell and Smith, 1982). The data (Figure 2) show that InsP6, EDTA and Desferral all fall into this category; the greater potency of InsP6 compared with the other two chelators is presumably because InsPJ has multiple phosphates which are capable of chelating Fe3+ with high affinity (i.e. more than one Fe3+ can be bound per InsP6; Graf et al.,
1987)."
http://www.biochemj.org/bj/294/0929/2940929.pdf

Young people and those who need to replace red blood cells (women of child-bearing years, people who take aspirin, people who exercise a lot, etc.) apparently don't have a problem with too much iron. But men over 40 and post-menopausal women tend to accumulate too much. And inflammation resulting from this excess iron may be the cause of a whole host of problems beyond dementia, such as arterial sclerosis and heart disease.

By the way, intramuscular injections of Desferral [desferioxamine, desferrioxamine or desferal] have been shown to halt the progression of Alzheimer's disease. There is also an oral equivalent Deferasirox (Exjade, Novartis). See: McLachlan DR, Dalton AJ, Kruck TP, Bell MY, Smith WL, Kalow W, Andrews DF. "Intramuscular desferrioxamine in patients with Alzheimer's disease." Lancet. 1991 Jun 1;337(8753):1304-8.


Current protocol consists of:

TUDCA
NAC
Na-R-ALA
resveratrol
grape seed extract
gingko biloba
vitamin C
silymarin
curcumin
CDC choline
EPA/DHA
Coenzyme Q10
melatonin
B-complex
Methyl B-12
folic acid


Supplements that I would like to add:

Pyritinol
vincamine
Hydergine
Scyllitol

Note: considering EDTA for iron chelation

Peter LeDrew
03-02-2008, 05:29 PM
Current protocol consists of:

TUDCA
NAC
Na-R-ALA
resveratrol
grape seed extract
gingko biloba
vitamin C
silymarin
curcumin
CDC choline <----you mean CDP-Choline right?
EPA/DHA
Coenzyme Q10
melatonin
B-complex
Methyl B-12
folic acid


Supplements that I would like to add:

Pyritinol
vincamine
Hydergine
Scyllitol

Note: considering EDTA for iron chelation

Surprised no green tea extract here... some great nutrients though.
I think a potent Boswellia extract would go well here to deal with the 5-lipooxygenase pathway of inflammation. Lyprinol is supposedly amazing too.
http://www.aor.ca/int/related_research/maxi-boz.php

What about aspirin, even a 81mg daily dose may help with the low dose reducing risk of problems.

And about the iron. It can be especially a problem for men and that is why donating blood is great for men in reducing a build up of iron...

One of the studies you posted on iron talked about the potential of iron chelators... one of or the best found in nature IP6 has an indirect antioxidant effect through it's chelation of free iron, preventing the formation of damaging hydroxyl radicals. It also chelates other minerals, manganese likely too.
http://www.aor.ca/int/related_research/ip6.php

As you can see AOR provides many answers in the quest for longevity and disease prevention. Great company and very professional/science based.
Their Ortho Core multi provides many of the ingredients needed for optimum health. I take 1-2 with every meal.

Hope you got something out of my post anyways.

Peter LeDrew
03-02-2008, 05:35 PM
Have you considered IP6? I've been giving my mother about 800mg of IP6 (on an empty stomach) for about a year now. Originally we thought she had AD. But since I read the article about "Parkinsonain Syndromes" and iron metabolism ("Inhibition of iron-Iron metabolism in Parkinsonian syndromes" Mov Disord. 2006 Sep;21(9):1299-310. http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=16817199&cmd=showdetailview
However, I'm not sure how much to give her. The IP6 I buy is actually sold as an immune system booster, and for that they take it in grams!

Here's an article about IP6...
"Inhibition of iron-catalysed hydroxyl radical formation by inositol polyphosphates: a possible physiological function for myo-inositol hexakisphosphate"
Phillip T. HAWKINS, David R. POYNER,* Trevor R. JACKSON, Andrew J. LETCHER, David A. LANDER and Robin F. IRVINE Department of Biochemistry, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge CB2 4AT, U.K.

"In 1984, Graf et al. showed that InsP. was a particularly effective inhibitor of iron-catalysed hydroxyl radical (OH') formation, and suggested that it might make a useful food additive (Graf et al., 1984, 1987; Graf and Eaton, 1990)."

"Some idea of the relative affinity of InsP6 for Fe3+ was deduced by competition experiments measuring the decolorization of FeCl3/catechol complexes (see the Materials and methods section). Any compound that is able to compete with catechol for Fe3+ in the same concentration range as the Fe'+-catechol complex (0.25 mM in this case) must have an affinity for Fe3+
that is of a similar order to, or greater than, that of catechol (the K1 for which is approx. 10-20; Martell and Smith, 1982). The data (Figure 2) show that InsP6, EDTA and Desferral all fall into this category; the greater potency of InsP6 compared with the other two chelators is presumably because InsPJ has multiple phosphates which are capable of chelating Fe3+ with high affinity (i.e. more than one Fe3+ can be bound per InsP6; Graf et al.,
1987)."
http://www.biochemj.org/bj/294/0929/2940929.pdf

Young people and those who need to replace red blood cells (women of child-bearing years, people who take aspirin, people who exercise a lot, etc.) apparently don't have a problem with too much iron. But men over 40 and post-menopausal women tend to accumulate too much. And inflammation resulting from this excess iron may be the cause of a whole host of problems beyond dementia, such as arterial sclerosis and heart disease.

By the way, intramuscular injections of Desferral [desferioxamine, desferrioxamine or desferal] have been shown to halt the progression of Alzheimer's disease. There is also an oral equivalent Deferasirox (Exjade, Novartis). See: McLachlan DR, Dalton AJ, Kruck TP, Bell MY, Smith WL, Kalow W, Andrews DF. "Intramuscular desferrioxamine in patients with Alzheimer's disease." Lancet. 1991 Jun 1;337(8753):1304-8.

Great post! btw, when I posted mine, I did not see this and I can't believe how we hit on many of the same points. Cool. :)

Did your mom benefit from the IP6 protocol?

DRP7
03-03-2008, 01:29 AM
@ swarfmaker & PeterLeDrew:

very good posts! some years ago a Japanese antibiotic drug (forgot the name) was found to have extremely potent chelating properties in the brain and to significantly impact alzheimer's pathology in mouse models.

I didn't know that IP6 might have similar properties. Does it cross the blood brain barrier?

swarfmaker
03-04-2008, 08:15 PM
This is a good question that I don't remember the answer to, and I've been meaning to look it up. I've read an awful lot in the last two years, and things are starting to blur.

On a related topic, I just found out today that there is some significant research suggesting that lithium may protect neurons from tau protein damage. Lithium carbonate is commonly prescribed to people with bipolar disorder to help with their mood swings. However, I found that lithium orotate is available at health food stores. Real sea salt also contains trace amounts of lithium. For bipolar disorder, the lithium levels have to be kept between narrow margins so as to be effective without being toxic. I don't know how much lithium one would need in one's diet to prevent or treat dementia caused by tau proteins (Parkinson's, DLB, PSP, CBG, etc.) I'm still looking into this.

I think I'll start using sea salt instead of regular processed salt.

It's too bad about too much iron not be good for your health. I love the stuff. I mean... my alias, "Swarfmaker" is derived from the British term for swarf: "small chips of metal". I take large, expensive pieces of steel and turn them into small, worthless chips. for a hobby.


@ swarfmaker & PeterLeDrew:

very good posts! some years ago a Japanese antibiotic drug (forgot the name) was found to have extremely potent chelating properties in the brain and to significantly impact alzheimer's pathology in mouse models.

I didn't know that IP6 might have similar properties. Does it cross the blood brain barrier?

swarfmaker
03-05-2008, 07:41 PM
ALS, commonly known as "Lou Gehrig's Disease" has some relation to the dementias discussed.

Here is a the PubMed abstract about lithium:

PubMed ID: 18250315

"ALS is a devastating neurodegenerative disorder with no effective treatment. In the present study, we found that daily doses of lithium, leading to plasma levels ranging from 0.4 to 0.8 mEq/liter, delay disease progression in human patients affected by ALS. None of the patients treated with lithium died during the 15 months of the follow-up, and disease progression was markedly attenuated when compared with age-, disease duration-, and sex-matched control patients treated with riluzole for the same amount of time. In a parallel study on a genetic ALS animal model, the G93A mouse, we found a marked neuroprotection by lithium, which delayed disease onset and duration and augmented the life span. These effects were concomitant with activation of autophagy and an increase in the number of the mitochondria in motor neurons and suppressed reactive astrogliosis. Again, lithium reduced the slow necrosis characterized by mitochondrial vacuolization and increased the number of neurons counted in lamina VII that were severely affected in saline-treated G93A mice. After lithium administration in G93A mice, the number of these neurons was higher even when compared with saline-treated WT. All these mechanisms may contribute to the effects of lithium, and these results offer a promising perspective for the treatment of human patients affected by ALS."

Try this link
http://www.pnas.org/cgi/content/full/105/6/2052

swarfmaker
06-08-2008, 05:21 AM
This is just astounding news. There is apparently a water-soluble extract of commonly available cinnamon (cassia cinnamon or Chinese cinnamon) that inhibits the aggregation of tau proteins AND will actually untangle "fibers" that have already formed! (Search Wikipedia for "cassia cinnamon".)

For those not familiar with neurodegenerative diseases, corruption of the tau proteins inside of neurons is thought to be a cause, or at least a major step, of several diseases. What this means is that if tau is involved, this cinnamon extract may be a means to halting the disease!

I have read several reports from people caring for people with Alzheimer's disease that have seen amazing results from a cinnamon supplement protocol. 1000mg, 3x per day of cassia cinnamon capsules (widely available at stores like Target, WalMart, etc.) Saliva enzymes degrade the cinnamon, but stomach acid neutralizes the saliva enzymes, so capsules are the way to go. But don't overdue it either. There are some toxic substances in whole cinnamon that could be detrimental if someone were to take too much for too long. The toxins are mostly in the fat-soluble parts, so making a "cinnamon tea" extracts the water-soluble components.

Cinnamon has also been found to help people regulate sugar metabolism, and some use it control type II diabetes. Taking cinnamon supplements has also been reported to lower cholesterol levels by as much as 60 points.

I NEVER expected to find something available in grocery stores that might actually be able to halt neurodegenerative diseases.

The greatest risk factor for these diseases is age. At some point, you will have to deal with it. It may be a grand parent, parent, or spouse's parent that is afflicted, and even if you are relatively young and healthy, your life will be turned upside down as you deal with being a caregiver. Maybe this common spice can save you from this fate.

Search the Internet for "tau" and "cinnamon" and "alzheimer". for more information.

Phosphate bond
06-08-2008, 08:55 AM
also, the role of mitochondrial dysfunction and insulin sensitivity are issues that are "hot-topics" in current AD-research. So, it would be worth to try supplements that improve both pathways.


That is interesting. I actually do think stable insulin function and stable insulin levels do have link in the brain.

Phosphate bond
06-08-2008, 09:00 AM
very good posts! some years ago a Japanese antibiotic drug (forgot the name) was found to have extremely potent chelating properties in the brain and to significantly impact alzheimer's pathology in mouse models.




Deficient Cysteine formation (from the conversion of homocysteine) might be involved here too. Of course cysteine chelates iron and copper, etc.

Actually chelated iron and copper play essential roles in cytochromes and krebs cycle enzymes. If this doesn't occur energy production is stunted and all kinds of by-products build-up.

I actually think all this stuff is tied together with insulin function. (Long story).

To convert homocysteine to cysteine you need serine. Serine availability is going to be poor anytime NADH is built-up.

Phosphate bond
06-08-2008, 09:06 AM
- DHA (not EPA!)


DHA increases phosphatidylserine formation.

I think this is one reason why it is known to help certain chelating problems.

That serine when liberated could be used to form cysteine out of homocysteine.

Of course if NADH is build-up from other problems in the body that serine could be converted back to glycine. (serine + NADH----> glycine). Then it is a "wash".

DRP7
06-12-2008, 03:23 AM
DHA increases phosphatidylserine formation.




my reasoning on DHA came from in vitro and animal studies that show a direct involvement of DHA in regulation of cellular cholesterin production/homeostasis. it acts in a similar way as a HMB-inhibitor, and cholesterin production (in the neuron) is closely related to amyloid beta production.

NO HYPE
06-12-2008, 04:04 AM
JAMA Vol. 299 No. 22, 2642-2655. June 11, 2008
Rixt F. Riemersma-van der Lek, MD; Dick F. Swaab, MD, PhD; Jos Twisk, PhD; Elly M. Hol, PhD; Witte J. G. Hoogendijk, MD, PhD; Eus J. W. Van Someren, PhD

Effect of Bright Light and Melatonin on Cognitive and Noncognitive Function in Elderly Residents of Group Care Facilities

A Randomized Controlled Trial

Context
Cognitive decline, mood, behavioral and sleep disturbances, and limitations of activities of daily living commonly burden elderly patients with dementia and their caregivers. Circadian rhythm disturbances have been associated with these symptoms.

Objective
To determine whether the progression of cognitive and noncognitive symptoms may be ameliorated by individual or combined long-term application of the 2 major synchronizers of the circadian timing system: bright light and melatonin.

Design, Setting, and Participants
A long-term, double-blind, placebo-controlled, 2 x 2 factorial randomized trial performed from 1999 to 2004 with 189 residents of 12 group care facilities in the Netherlands; mean (SD) age, 85.8 (5.5) years; 90% were female and 87% had dementia.

Interventions
Random assignment by facility to long-term daily treatment with whole-day bright (? 1000 lux) or dim (? 300 lux) light and by participant to evening melatonin (2.5 mg) or placebo for a mean (SD) of 15 (12) months (maximum period of 3.5 years).

Main Outcome Measures
Standardized scales for cognitive and noncognitive symptoms, limitations of activities of daily living, and adverse effects assessed every 6 months.

Results
Light attenuated cognitive deterioration by a mean of 0.9 points (95% confidence interval [CI], 0.04-1.71) on the Mini-Mental State Examination or a relative 5%. Light also ameliorated depressive symptoms by 1.5 points (95% CI, 0.24-2.70) on the Cornell Scale for Depression in Dementia or a relative 19%, and attenuated the increase in functional limitations over time by 1.8 points per year (95% CI, 0.61-2.92) on the nurse-informant activities of daily living scale or a relative 53% difference. Melatonin shortened sleep onset latency by 8.2 minutes (95% CI, 1.08-15.38) or 19% and increased sleep duration by 27 minutes (95% CI, 9-46) or 6%. However, melatonin adversely affected scores on the Philadelphia Geriatric Centre Affect Rating Scale, both for positive affect (?0.5 points; 95% CI, ?0.10 to ?1.00) and negative affect (0.8 points; 95% CI, 0.20-1.44). Melatonin also increased withdrawn behavior by 1.02 points (95% CI, 0.18-1.86) on the Multi Observational Scale for Elderly Subjects scale, although this effect was not seen if given in combination with light. Combined treatment also attenuated aggressive behavior by 3.9 points (95% CI, 0.88-6.92) on the Cohen-Mansfield Agitation Index or 9%, increased sleep efficiency by 3.5% (95% CI, 0.8%-6.1%), and improved nocturnal restlessness by 1.00 minute per hour each year (95% CI, 0.26-1.78) or 9% (treatment x time effect).

Conclusions
Light has a modest benefit in improving some cognitive and noncognitive symptoms of dementia. To counteract the adverse effect of melatonin on mood, it is recommended only in combination with light.

Phosphate bond
06-12-2008, 08:11 AM
my reasoning on DHA came from in vitro and animal studies that show a direct involvement of DHA in regulation of cellular cholesterin production/homeostasis. it acts in a similar way as a HMB-inhibitor, and cholesterin production (in the neuron) is closely related to amyloid beta production.

That is interesting. (I learn something everyday)

Yeah I mentioned the Homocysteine lowering effects (to cysteine) because "chelation" was being mentioned here.

ElMariachi
06-12-2008, 08:54 AM
Phospatidyl Serine and DHA although I haven't read through the whole thread so I'm sure that someone has mentioned them.

swarfmaker
04-06-2009, 09:39 AM
It's been a while since I visited. Some interesting developments have occurred. I can list the references for anyone interested, but you can easily find out more about them by searching on Google.

This is for those who either are looking to prevent dementia or are now facing the problem of having a parent with a dementing illness like Alzheimers, etc.

Check out the recent developments using "medium chain triglycerides". Search for keywords like "Dr. Mary Newport", coconut oil, caprylic acid, Alzheimer's disease. I'm sure that folks here are well aware of the various MCT supplements such as TwinLabs's "MCT Fuel", Ultimate Nutrition's "MCT Gold", etc. These substances have shown a remarkable positive effect on people with Alzheimer's. If you are faced with the problem of caring for someone with AD, you will want to know more about these things.

Also, some other substances you will want to investigate: cinnamon proanthocyanidins (search on that and Dr. Graves and Alzheimer), niacinamide, and methlyene blue. Also, you may want to check out "high dose" (~2400mg/day) CoQ10.

I hope you find this information useful.

LactoseTolerant
04-06-2009, 11:11 AM
Slightly off the track of this discussion but I'm sure many of you have heard the theory linking Alzheimer's and diabetes:

http://www.salk.edu/news/pressrelease_details.php?press_id=221

vexxdone
04-06-2009, 01:01 PM
i wish i couldve had a chance to read this thread a couple years ago when when my grandfather suffered from dementia (and the rest of us). Thanks for the information

Wearwolf51
04-06-2009, 04:55 PM
I didnt have time to read the whole thread but I just wanted to give you props for what you are doing, I will use the information that is here to help anyone that I know suffering from dementia in the future. Thank you.

Also I was wondering have you integrated Vinpocetine into his supplement protocol, I know it is used by many for its aid in memory. Another thing that struck me as a good idea was Pregnenolone.

Sorry if these have already been mentioned, hope things are looking up for him and you.

ragamuffinsaint
04-09-2009, 07:55 AM
Are there any good big radomised control trials out there on this? these obviously need to be carried out to draw any real conclusions - problem though is that are you goin to withhold other proven treatment while on this regime? Ethically you wouldnt get away with that.

NO HYPE
04-10-2009, 05:02 AM
the role of mitochondrial dysfunction and insulin sensitivity are issues that are "hot-topics" in current AD-research. So, it would be worth to try supplements that improve both pathways.


Deficient Cysteine formation (from the conversion of homocysteine) might be involved here too.

After extensively researching the degree and/or impact of age-related total glutathione depletion, there is absolutely no doubt in my mind that properly-dosed GSH-enhancing supplements [like NAC/Na-RALA/SAMe, ect.] are of significant benefit for ameliorating the impact of cognitive decline, and they effectively address the degree of mitochondrial dysfunction and deficient cysteine formation related to the disease. Additionally, I believe brain GSH-depletion in particular, is a very serious factor in the pathogenesis of AD and/or dementia.




i wish i couldve had a chance to read this thread a couple years ago when when my grandfather suffered from dementia (and the rest of us). Thanks for the information


I didnt have time to read the whole thread but I just wanted to give you props for what you are doing, I will use the information that is here to help anyone that I know suffering from dementia in the future. Thank you.

No problem. I'm glad I could be of help.




Also I was wondering have you integrated Vinpocetine into his supplement protocol, I know it is used by many for its aid in memory. Another thing that struck me as a good idea was Pregnenolone.

I'll look into this. Thanks for the suggestions.




hope things are looking up for him and you.

They are. I have managed to [effectively and significantly] slow the progression of my dad's disease. It is rather apparent when you deal with this disease on a daily basis. Thank you for the concern.

dirkwright
04-14-2009, 04:56 AM
I just wanted to take a few minutes, not to discuss dementia as a disease, but to discuss the supplements which I have incorporated into my father's daily supplemental protocol, that have demonstrated unequivocal efficacy in the alleviation of his symptoms. Additionally in my opinion, I STRONGLY feel that these antioxidants when taken regularly, will significantly reduce the risk of developing this disease.

....

I truly hope that this information reaches anyone who is unaware of these facts.

Thank you. My Mom died from AD at age 67. She was diagnosed at 62. I am not like her, more like my Dad's side of the family, but I still take a bunch of stuff for my brain.

I take piractam with ALA, Alpha GPC and choline, in addition to many of the supplements you mentioned. I've had my amalgams replace with non-metallic ones, and did cheltation therapy afterwards. I did a hair analysis that showed low levels of heavy metals. I think I'm ok so far. I feel smart anyway.

I'm considering adding SAMe to my supplements, but I read somewhere that we need to take B vitamins with it to prevent the accumulation of homocysteine. http://www.biopsychiatry.com/sameart.html
I found a product that is a complex of B vitamins and SAMe, but it only has 25 mg of SAMe. Is that enough to help?:

"Assuming you buy full-strength SAMe, the second challenge is to use it effectively. Experts advise taking it twice a day on an empty stomach, but different people may require different amounts. Though studies suggest that 400 mg a day is an effective dose for arthritis, the daily doses used in depression trials have ranged as high as 1,600 mg. Clinicians generally start people with mood problems at 400 and ratchet up as necessary. " from a 1999 Newsweek article.

So, taking SAMe in 400 mg enteric coated tablets with folic acid, B6 and B12 looks important.

dirkwright
04-14-2009, 05:24 AM
REM Sleep Behavior Disorder: Harbinger of Synucleinopathies?[/B]
Charles J. Ippolito, MD


"We also have had some success with ramelteon [Rozerem], which is a new melatonin receptor agonist, and it seems to be effective especially in refractory cases," Boeve continued. Alternative treatments recommended by Boeve include quetiapine (Seroquel) and sodium oxybate (Xyrem), although he cautioned that impaired cognition is an adverse effect of the latter. "Overall, I would rank clonazepam as number 1 in treating RBD and melatonin as number 2, followed by a smattering of other medications that can be tried on an individual patient basis," he concluded.

http://www.appneurology.com/showArticle.jhtml?articleId=193104734

I've tried Rozerem, and I liked it. It's just really expensive and my insurance doesn't cover it. I didn't do any kind of objective measurements though. Getting a good night's sleep is critical to getting a good workout the next day, I have found. So, what ever it takes to knock my out for a long time is what I do.

UNCnate
10-25-2009, 12:24 PM
Bumping an old thread, but there is a lot of good information in here.

Im considering getting my grandfather to start supplementing with some of these protocols.

DR_P
10-25-2009, 01:19 PM
Bumping an old thread, but there is a lot of good information in here.

Im considering getting my grandfather to start supplementing with some of these protocols.


as from my most current insight, I would recommend the following blend for preventive purposes and long-term intake. Except for some very special cases, this is very well tolerated and should not have any relevant adverse effects. (this does not apply to patients on anticoagulation medication sucha s warfarin, who might get an increased risk of bleedings).


- 600 mg of ALA
- 500 mg of curcumin with every meal (3 x /d)
- a good, not too high dosed soy phospholipid product
- alphatocopherolsuccinate (200 mg/d) + 20-50 mg tocotrienols



Do you guys want to know what's getting studied in phase I/II for Alzheimer's?



METHYLENBLUE (!!!!)

Couldn't believe it myself, but REMBER (fancy code name / brand name for methyleneblue) appears extremely promising in fighting tauopathies and AD.

It's widely available (not in pharmacy of course). Who is interested may look up the dosing protocol used in the most recent REMBER phase II study. Personally, I believe its overdosed in that study. It appears to be well tolerated (except that it taints your eyes blue, lol, and of course some gastrointestinal issues, as usual).


Another completely surprising substance is Dimebone (an old russian antihistaminic that got forgotten for decades, but some smart mofo remebered to dig it up); last year the results of a recent large, controlled, multicenter study (phase II) got published and - although not yet on the market - it already gained status of the "next thing" after the Cholineesterase-inhibitors. It appears to beat them hands down.

The absolutely newest thing is a g-secr. inhibitor from Lilly. It's in phase II or III right now - and - in some individual patients - it appears to work wonders. Can you imagine when a patient with seere dementia, who is not even able to talk anymore, let alone to comprehend anything, suddenly starts to be active, to talk, to be much more attentive etc. Well, it's individual cases where it works so well, but the effects are shocking, to say the least.

UNCnate
10-25-2009, 01:31 PM
I had heard about the methylene blue idea. Some people at the immortality institute forum have been using it.

Are people not recommending huperzine A anymore?

My grandfather is on several medications right now, warfarin being one of them. I need to check the laundry list of all of them. Having had two heart attacks, seizures, and dementia, he is on plenty.

I was hoping to get together some research/ideas to have him/my grandmother speak to the doc about on the next follow up.

DR_P
10-25-2009, 02:09 PM
I had heard about the methylene blue idea. Some people at the immortality institute forum have been using it.

Are people not recommending huperzine A anymore?

My grandfather is on several medications right now, warfarin being one of them. I need to check the laundry list of all of them. Having had two heart attacks, seizures, and dementia, he is on plenty.

I was hoping to get together some research/ideas to have him/my grandmother speak to the doc about on the next follow up.


1. how old is he?
2. who made the dementia diagnosis (GP or neurologist/psychiatris)?
3. What kind of dementia is it (vascular, Alezheimer's, mixed-type, frontal, etc...)?
4. what is his CURRENT state of disability? What activities of daily living is he able to do alone?
5. Is he already on any dementia medication?
6. What are his other diagnoses and meds? particularly, does he suffer from arrhytmia?


these are just SOME of critical data that must be known before putting anyone on ANY kind of medication.

UNCnate
10-25-2009, 02:19 PM
1. how old is he?
2. who made the dementia diagnosis (GP or neurologist/psychiatris)?
3. What kind of dementia is it (vascular, Alezheimer's, mixed-type, frontal, etc...)?
4. what is his CURRENT state of disability? What activities of daily living is he able to do alone?
5. Is he already on any dementia medication?
6. What are his other diagnoses and meds? particularly, does he suffer from arrhytmia?


these are just SOME of critical data that must be known before putting anyone on ANY kind of medication.

I will find out more of this.

1) 62
2) Neurologist
3) Vascular, I believe. Will find out.
4) He is actually still very active. He has problems with memory sometimes, but nothing as far as coordination, etc.
5) I believe so, will find out.
6) Will find out.

I found this thread after a conversation with my mom the other day. He was in a car wreck in the 70's, has had seizures since. I was wondering if the seizures are causing his dementia, or if it was genetic. She wasnt sure. I was telling her we need to find out, because if it is genetic we need to assess everyones risk factors and get the family on a preventative protocol.

I need to try to get more of a history here.

Achilles_1986
05-14-2010, 07:03 PM
Bumping this as I was looking for info on Alpha GPC and came across this thread.

First and foremost, Hype how is your father? This thread is a wealth of knowledge and I will have to re-read a few times.

I extend prayers for you and your family, I lost my grandmother when I was around 12-13 years of age to Alzheimer's disease and been searching and reading as much as I can to prevent this disease for myself and others. The protocols laid are great btw!

VegasLife
05-23-2010, 05:02 PM
Great thread. Subbed for updates.

Glad to hear that your dad responded so well.

krazykarl
05-24-2010, 02:34 PM
sub'd.

G.W. Hayduke
06-03-2010, 12:56 AM
Marijuana might cause new cell growth in the brain : http://www.newscientist.com/article/dn8155-marijuana-might-cause-new-cell-growth-in-the-brain.html
(This shows that endocannabinoids are important in neurogenesis: http://www3.interscience.wiley.com/journal/119409848/abstract?CRETRY=1&SRETRY=0)


Education Helps Against Dementia, Swedish Study Finds: http://www.sciencedaily.com/releases/2010/05/100531082855.htm

DR_P
06-06-2010, 04:29 AM
Marijuana might cause new cell growth in the brain : http://www.newscientist.com/article/dn8155-marijuana-might-cause-new-cell-growth-in-the-brain.html
(This shows that endocannabinoids are important in neurogenesis: http://www3.interscience.wiley.com/journal/119409848/abstract?CRETRY=1&SRETRY=0)


Education Helps Against Dementia, Swedish Study Finds: http://www.sciencedaily.com/releases/2010/05/100531082855.htm


Education has less adverse effects compared with Marijuana.

aoba
06-15-2010, 08:48 AM
There's actually a study going on down here soon about some kind of "whole foods" replacement supplement with vit E/C and gingko and its effect on cognition in 60+ year olds...they're measuring quite a few things other than just a using a cognition battery of tests..i think they're also looking at inflammatory cytokines.

NO HYPE
06-15-2010, 09:05 AM
i think they're also looking at inflammatory cytokines.

Speaking of inflammatory cytokines, amyloid-b peptide is a potent activator of NF-kB [the master regulator of inflammation]. I am so thankful to have nutraceuticals that effectively diminish the presence of excessive NF-kB transcription. If only I would have known this in the years prior to my father's diagnosis.

G.W. Hayduke
06-15-2010, 10:04 AM
Education has less adverse effects compared with Marijuana.

Well then, I guess education ftw.

/thread

NO HYPE
06-15-2010, 10:37 AM
Education has less adverse effects compared with Marijuana.

I wonder if the same would apply to ingested trichomes --> the primary housing of the plant's THC content [which is void of the plant matter]?

DR_P
06-15-2010, 12:31 PM
There's actually a study going on down here soon about some kind of "whole foods" replacement supplement with vit E/C and gingko and its effect on cognition in 60+ year olds...they're measuring quite a few things other than just a using a cognition battery of tests..i think they're also looking at inflammatory cytokines.

Gingko, Vit C and E?

won't hurt but won't even help much either, I guess.

NO HYPE
06-15-2010, 12:46 PM
Gingko, Vit C and E?

won't hurt but won't even help much either, I guess.

Well at least Ginkgo biloba should enhance cerebral blood flow, and the vitamin c [combined with NAC] should effectively diminish cerebral glutathione depletion however, I don't see much use for the vitamin e.

aoba
06-15-2010, 03:12 PM
Gingko, Vit C and E?

won't hurt but won't even help much either, I guess.

Yeah I haven't really looked into it since it's for 60+ only..but if anyone around Miami that wants to be compensated for their time in that age range I can point them in the right direction.

papagunz
06-15-2010, 03:40 PM
I don't see much use for the vitamin e.

Pretty sure it has been shown to mitigate oxidative stress from the beta-amyloid plaques, at least to some degree.

Actually: http://www.ncbi.nlm.nih.gov/pubmed/10658956

I know it's an abstract (to illustrate my point), but it (vitamin e mitigating peroxidation damage, ect) did come up a few times during my research on AD for my neuro midterm paper.

NO HYPE
06-16-2010, 01:44 AM
Pretty sure it has been shown to mitigate oxidative stress from the beta-amyloid plaques, at least to some degree.

Actually: http://www.ncbi.nlm.nih.gov/pubmed/10658956

I know it's an abstract (to illustrate my point), but it (vitamin e mitigating peroxidation damage, ect) did come up a few times during my research on AD for my neuro midterm paper.

Thank you for the insight [repped]. Since Abeta-associated free radical oxidative stress appears to be a decisive factor in AD neurotoxicity, I would be inclined to assume that the combination of NAC and vitamin c would have a more pronounced impact on significantly diminishing cerebral oxidative stress and/or neurotoxicity, as decrements in cerebral glutathione are a well-known factor in both diseased and non-diseased individuals.

papagunz
06-17-2010, 10:29 AM
Also, I don't recall either vitamin D or glutamate excitotoxicity being mentioned here either. As far as I know, AB plaques have been shown to inhibit GLT-1 and GLAST, leading to another moa for neurotoxicity. Yay.

De__eB
06-21-2010, 11:43 AM
Ajoene, a Stable Garlic By-Product, Has an Antioxidant Effect through Nrf2-Mediated Glutamate-Cysteine Ligase Induction in HepG2 Cells and Primary Hepatocytes (http://jn.nutrition.org/cgi/content/short/140/7/1211?rss=1)

Our results demonstrate that ajoene increases PKC-dependent Nrf2 activation, GCL induction, and the cellular GSH (Glutathione) concentration, which may contribute to protecting cells from oxidative stress.

Any use to you?

papagunz
06-21-2010, 02:46 PM
Ajoene, a Stable Garlic By-Product, Has an Antioxidant Effect through Nrf2-Mediated Glutamate-Cysteine Ligase Induction in HepG2 Cells and Primary Hepatocytes (http://jn.nutrition.org/cgi/content/short/140/7/1211?rss=1)

Our results demonstrate that ajoene increases PKC-dependent Nrf2 activation, GCL induction, and the cellular GSH (Glutathione) concentration, which may contribute to protecting cells from oxidative stress.

Any use to you?

Just reading the title, its talking about liver cells. The importance of increasing glutathione has been made apparent by No Hype, but whether this pertains to neuronal cells I am unsure. I'll read the article sometime here soon.

Anyway, I am more aimed at looking at mitigating the AB induced changes in GLT-1 and GLAST (glutamate transporters) to reduce the effects of glutamate excitotoxicity.

NO HYPE
06-21-2010, 03:09 PM
Ajoene, a Stable Garlic By-Product, Has an Antioxidant Effect through Nrf2-Mediated Glutamate-Cysteine Ligase Induction in HepG2 Cells and Primary Hepatocytes (http://jn.nutrition.org/cgi/content/short/140/7/1211?rss=1)

Our results demonstrate that ajoene increases PKC-dependent Nrf2 activation, GCL induction, and the cellular GSH (Glutathione) concentration, which may contribute to protecting cells from oxidative stress.

Any use to you?

Thank you for the heads up. Unfortunately, the instability of allicin requires isolation via thin layer chromatography which limits it's commercial availability. The allicin condensation product [ajoen] aquires more antiviral activity in general than allicin itself. In respect to any over-the-counter allicin/ajoen products, aqueous extracts of ajoens are [significantly] more abundant in vinildithiins and dialkenyl sulfides than ethanol extracts. In any case [as mentioned previously], "I would be inclined to assume that the combination of NAC and vitamin c would have a more pronounced impact on significantly diminishing cerebral oxidative stress and/or neurotoxicity, as decrements in cerebral glutathione are a well-known factor in both diseased and non-diseased individuals."

For what it's worth, there is a commercially available product called Allicillin Pro, by Designs for Health which does in fact provide ajoene standardized to 1%.

NO HYPE
06-21-2010, 03:13 PM
The importance of increasing glutathione has been made apparent by No Hype, but whether this pertains to neuronal cells I am unsure.

Indeed it does my friend [as I'm sure you will find out within the literature]. :)

NO HYPE
06-21-2010, 03:14 PM
Anyway, I am more aimed at looking at mitigating the AB induced changes in GLT-1 and GLAST (glutamate transporters) to reduce the effects of glutamate excitotoxicity.

Please keep us updated. Much appreciated.

Roke
06-22-2010, 09:02 PM
That's an excellent cocktail of anti-oxidants.

B-Vitamins, spirulina are excellent for the brain.

JornT
07-19-2010, 07:28 AM
Pretty sure it has been shown to mitigate oxidative stress from the beta-amyloid plaques, at least to some degree.

Actually: http://www.ncbi.nlm.nih.gov/pubmed/10658956

I know it's an abstract (to illustrate my point), but it (vitamin e mitigating peroxidation damage, ect) did come up a few times during my research on AD for my neuro midterm paper.

I came across this recent cohort on vitamin E rich [foods] and dementia risk.

http://archneur.ama-assn.org/cgi/content/short/67/7/819

papagunz
07-19-2010, 03:20 PM
Please keep us updated. Much appreciated.

The more I read the more I see that the conformational changes in glutamate transporters are due to oxidative stress et al. So, looks like you are on point with the glutathione agonism. I would also suggest a B complex to mitigate hyperhomocysteinemia as one of homocysteine's metabolites can agonize the NMDA receptor. (and, people with dementia afaik are typically B vitamin deficient)

Sorry I don't have anything really groundbreaking to offer. If you'd like I can email you my term paper from last semester. You probably won't learn much but it'd be a good "flesher outer." No pressure, only if you're interested.

NO HYPE
09-03-2010, 08:56 AM
I just wanted to take this oppertunity to thank all of the forum members that have contributed to this thread from the bottom of my heart. Unfortunately, my Father lost his 5-year battle with dementia this morning, and this has truly been the most difficult predicament that I have ever encountered in my life. I simply can't stress enough the fact that starting a glutathione-enhancing protocol [early on in life] is one of the most crucial life-enhancing steps an individual can take in an effort to make the most out of life. I only wish I had been aware of this in the years prior to my Fathers diagnosis.

I would be inclined to assume that the combination of glutathione-enhancing compounds like NAC/SAMe/Na-RALA/vitamin C, ect. would have a more pronounced impact on significantly diminishing cerebral oxidative stress and/or neurotoxicity, as decrements in cerebral glutathione are a well-known factor in both diseased and non-diseased individuals.

After extensively researching the degree and/or impact of age-related total glutathione depletion, there is absolutely no doubt in my mind that properly-dosed GSH-enhancing supplements are of significant benefit for ameliorating the impact of cognitive decline, and they effectively address the degree of mitochondrial dysfunction and deficient cysteine formation related to the disease. Additionally, I believe brain GSH-depletion in particular, is a very serious factor in the pathogenesis of AD and/or dementia, as glutathione levels are chronically compromised/depleted, under various circumstances. Some of these factors include age and disease-related decrements, environmental toxins, excessive oxidative stress ect. For example, it has been documented that a 37 % decrease in brain GSH can occur following chronic stress exposure alone [lost the citation].



Expert Rev Neurother. 2008 Jan;8(1):133-58.
Lifestyle-related factors in predementia and dementia syndromes.

Studies in the literature seem to identify in physical exercise one promising strategy in decreasing cognitive decline, but some of the limitations of these studies do not allow us to draw definite conclusions. At present, in older subjects, healthy diets, antioxidant supplements, the prevention of nutritional deficiencies, and moderate physical activity could be considered the first line of defense against the development and progression of predementia and dementia syndromes.

338lapuaAI
09-04-2010, 12:56 AM
I just wanted to take this oppertunity to thank all of the forum members that have contributed to this thread from the bottom of my heart. Unfortunately, my Father lost his 5-year battle with dementia this morning, and this has truly been the most difficult predicament that I have ever encountered in my life. I simply can't stress enough the fact that starting a glutathione-enhancing protocol [early on in life] is one of the most crucial life-enhancing steps an individual can take in an effort to make the most out of life. I only wish I had been aware of this in the years prior to my Fathers diagnosis.

Sorry to hear about the loss. My dad is starting to go through the same stuff right now but got a diagnosis about another condition he has also and it wasn't good news. Definitely know how you feel.

NO HYPE
09-05-2010, 09:00 PM
Sorry to hear about the loss. My dad is starting to go through the same stuff right now but got a diagnosis about another condition he has also and it wasn't good news. Definitely know how you feel.

Thank you. I'm not sure what your dad was diagnosed with, but I'm sure a glutathione-enhancing protocol would be of great benefit to him [as well as yourself]. PM me if you have any questions. Thanks again.

Peter LeDrew
09-05-2010, 09:04 PM
I just wanted to take this oppertunity to thank all of the forum members that have contributed to this thread from the bottom of my heart. Unfortunately, my Father lost his 5-year battle with dementia this morning, and this has truly been the most difficult predicament that I have ever encountered in my life. I simply can't stress enough the fact that starting a glutathione-enhancing protocol [early on in life] is one of the most crucial life-enhancing steps an individual can take in an effort to make the most out of life. I only wish I had been aware of this in the years prior to my Fathers diagnosis.

I would be inclined to assume that the combination of glutathione-enhancing compounds like NAC/SAMe/Na-RALA/vitamin C, ect. would have a more pronounced impact on significantly diminishing cerebral oxidative stress and/or neurotoxicity, as decrements in cerebral glutathione are a well-known factor in both diseased and non-diseased individuals.

After extensively researching the degree and/or impact of age-related total glutathione depletion, there is absolutely no doubt in my mind that properly-dosed GSH-enhancing supplements are of significant benefit for ameliorating the impact of cognitive decline, and they effectively address the degree of mitochondrial dysfunction and deficient cysteine formation related to the disease. Additionally, I believe brain GSH-depletion in particular, is a very serious factor in the pathogenesis of AD and/or dementia, as glutathione levels are chronically compromised/depleted, under various circumstances. Some of these factors include age and disease-related decrements, environmental toxins, excessive oxidative stress ect. For example, it has been documented that a 37 % decrease in brain GSH can occur following chronic stress exposure alone [lost the citation].



Expert Rev Neurother. 2008 Jan;8(1):133-58.
Lifestyle-related factors in predementia and dementia syndromes.

Studies in the literature seem to identify in physical exercise one promising strategy in decreasing cognitive decline, but some of the limitations of these studies do not allow us to draw definite conclusions. At present, in older subjects, healthy diets, antioxidant supplements, the prevention of nutritional deficiencies, and moderate physical activity could be considered the first line of defense against the development and progression of predementia and dementia syndromes.



Sorry to hear your loss... keep up the great work helping inform people here. When it comes to informed supplementation, I am on board with you.

NO HYPE
09-05-2010, 09:26 PM
Sorry to hear your loss... keep up the great work helping inform people here. When it comes to informed supplementation, I am on board with you.

Thank you so much Peter. Reps on recharge. I think being 34, not married, no children, and still feeling like I'm in my twenties has made this extremely hard for me [and I'm not saying this for a pitty-party either]. I honestly feel that had I known about enhancing glutathione expression and downregulating excessive NF-kB/TNF-a transcription in the years prior to my dad's diagnosis.... that it would have made a tremendous difference in the overall outcome. So if anyone can read this thread and get started early on in life, I truly believe that it will make a significant impact on one's quality of life.

stateless
09-06-2010, 06:33 AM
I'm very sorry to hear about this. I lost my Father when young and it can be painful to look back at all of the 'what ifs'. In time though, the fact that you are presenting people with opportunities to avoid such conditions will be very comforting for you. Keep up the good work in highlighting the importance of looking after your health. In this day and age, with scientific knowledge moving at a mile a minute, there's no excuse for young people to be ignorant of health issues.

Peter LeDrew
09-06-2010, 06:53 AM
Thank you so much Peter. Reps on recharge. I think being 34, not married, no children, and still feeling like I'm in my twenties has made this extremely hard for me [and I'm not saying this for a pitty-party either]. I honestly feel that had I known about enhancing glutathione expression and downregulating excessive NF-kB/TNF-a transcription in the years prior to my dad's diagnosis.... that it would have made a tremendous difference in the overall outcome. So if anyone can read this thread and get started early on in life, I truly believe that it will make a significant impact on one's quality of life.

There also needs to be a shift in thinking from the medical profession. You would think there would be more known about the possible benefits of disease prevention and treatment with such natural compounds. You're putting a lot of blame on yourself, when the bigger picture is what needs to be addressed. At least you are not ignorant to what is possible and by educating yourself you are doing what we all should be doing more. There are answers out there to these horrible diseases and like you, I do believe many of the answers lie in natural compounds and a less refined diet. You've likely helped many here, so keep up the good work in that regard.

papagunz
09-07-2010, 08:27 AM
No Hype, dementia runs in my family and I'm doing the best that I can to ensure your research will be put to good use. If no one else will regard it, I certainly will. At a minimum you've helped one person.

Thank you greatly and I am very sorry for your loss.

De__eB
09-07-2010, 08:45 AM
Sorry for your loss man.

Whenever you're in a state of mind to, could you write a cliffs of this thread and what your research came up with?

Perhaps an article about glutathione and the various support supplement regimens discussed? Would be a very useful piece of meta-information to have.

uforce
09-07-2010, 11:45 AM
Sorry for your loss man.

Whenever you're in a state of mind to, could you write a cliffs of this thread and what your research came up with?

Perhaps an article about glutathione and the various support supplement regimens discussed? Would be a very useful piece of meta-information to have.

^^i agree with this statement
i'm also sorry for your loss.

QuarterbackSack
09-09-2010, 01:03 AM
Very sorry about your loss, I wanted to post this study that was just completed. Sorry I cannot post the link. Still a few posts shy of being able to do that.

LONDON (Reuters) – Daily tablets of large doses of B vitamins can halve the rate of brain shrinkage in elderly people with memory problems and may slow their progression toward dementia, data from a British trial showed on Wednesday,

Scientists from Oxford University said their two-year clinical trial was the largest to date into the effect of B vitamins on so-called "mild cognitive impairment" -- a major risk factor for Alzheimer's disease and other forms of dementia.

Experts commenting on the findings said they were important and called for larger, longer full-scale clinical trials to see if the safety and effectiveness of B vitamins in the prevention of neurodegenerative conditions could be confirmed.

"This is a very dramatic and striking result. It's much more than we could have predicted," said David Smith of Oxford's department of pharmacology, who co-led the trial.

"It is our hope that this simple and safe treatment will delay development of Alzheimer's in many people who suffer from mild memory problems."

Mild cognitive impairment (MCI) affects around 16 percent of people aged over 70 worldwide and is characterized by slight problems with memory loss, language or other mental functions.

MCI does not usually interfere with daily life, but around 50 percent of people diagnosed with it go on to develop the far more severe Alzheimer's disease within five years. Alzheimer's is a mind-wasting disease for which there are few treatments and no cure, and which affects 26 million people around the world.

Smith and colleagues conducted a two-year trial with 168 volunteers with MCI who were given either a vitamin pill containing very high doses of folic acid, vitamin B6 and vitamin B12, or a placebo dummy pill.

These B vitamins are known to control levels of an amino acid called homocysteine in the blood, and high blood levels of homocysteine are linked to an increased risk of developing Alzheimer's disease.

Helga Refsum, who also worked on the trial, stressed that vitamins were given in extremely high doses.

"This is a drug, not a vitamin intervention," she said.

The pills, called "TrioBe Plus" contained around 300 times the recommended daily intake of B12, four times daily advised folate levels and 15 times the recommended amount of B6.

Brain scans were taken at the beginning and the end of the trial to monitor the rate of brain shrinkage, or atrophy.

The results, published in the Public Library of Science (PLoS) One journal, showed that on average the brains of those taking the vitamin treatment shrank at a rate of 0.76 percent a year, while those taking the dummy pill had an average brain shrinkage of 1.08 percent.

People who had the highest levels of homocysteine at the start of the trial benefited the most from the treatment, with their brains shrinking at half the rate of those on the placebo.

Although the trial was not designed to measure cognitive ability, the researchers found those people who had lowest rates of shrinkage had the highest scores in mental tests.

Commenting on the study, Paul Matthews, a professor of clinical neurology at Imperial College London said that although the vitamins used are generally safe and inexpensive, the study "should not drive an immediate change in clinical practice"

"Instead, it sets out important questions for further study and gives new confidence that effective treatments modifying the course of some dementias may be in sight," he said.

Achilles_1986
09-09-2010, 03:02 PM
Wow, sorry for your loss Hype, prayers extended to you and your loved ones mourning. I lost my grandmother to Alzheimer's, very sad to see what she went through.

Lucky_ROA
09-09-2010, 03:25 PM
Sorry for your loss NO HYPE :( May he rest in peace. Amen

NO HYPE
09-09-2010, 05:04 PM
I'm very sorry to hear about this.


Thank you greatly and I am very sorry for your loss.


Sorry for your loss man.


i'm also sorry for your loss.


Very sorry about your loss


Wow, sorry for your loss Hype, prayers extended to you and your loved ones mourning.


Sorry for your loss NO HYPE :( May he rest in peace. Amen

Thank you gentlemen.

collopy7
09-11-2010, 10:16 AM
Hey guys, I'm surprised to find this post on here. I started reading through your posts and just got too confused as I do not know a whole lot on this disease. I searched for dimentia because my grandmother, 82 years old, has dimentia. My mom is basically her caregiver. She's had dimentia for several years now, and it's getting worse. She's got kidney failure going on as well, and diabetes too. For dimentia, she's just getting dingy, ditzy, and confused often. She leaves the phone off the hook, mixes up where the bathroom is located...etc.
I told my mom I would come on here to look to see if there is anything recommended that she could maybe take to try and boost her memory or cut down on her dimentia symptoms. Is there anything you guys recommend or is it pointless?
I did find on a site recommending Phosphatidyl Serine. let me know your thoughts..
Thanks guys!

NO HYPE
09-11-2010, 11:03 AM
Hey guys, I'm surprised to find this post on here. I started reading through your posts and just got too confused as I do not know a whole lot on this disease. I searched for dimentia because my grandmother, 82 years old, has dimentia. My mom is basically her caregiver. She's had dimentia for several years now, and it's getting worse. She's got kidney failure going on as well, and diabetes too. For dimentia, she's just getting dingy, ditzy, and confused often. She leaves the phone off the hook, mixes up where the bathroom is located...etc.
I told my mom I would come on here to look to see if there is anything recommended that she could maybe take to try and boost her memory or cut down on her dimentia symptoms. Is there anything you guys recommend or is it pointless?
I did find on a site recommending Phosphatidyl Serine. let me know your thoughts..
Thanks guys!

Listen, the compounds discussed within this thread [which I encourage you to review one more time] are much more effective when administered [prior] to the years of this disease's diagnosis, however, it's never too late to start administering compounds that lessen the degree of the disease's symptoms. Just do not expect to see any amazing results pertaining to your grandmother at such a late stage of the disease. Do yourself a favor, and do not assume that because you're young and healthy that your quality of life will not significantly benefit in the years to come from initiating the supplementation of the compounds discussed within this thread. These compounds will not only effectively lessen the potential onset of Dementia, but also a plethora of other diseases. Glutathione enhancement and the downregulation of excessive NF-kb and TNF-a transcription are truly amazing physiological tools, and more people need to be aware of this fact.

mrbeverage
10-05-2010, 04:09 PM
this was just posted in Alliance of Naturual health.
http://www.anh-usa.org/coconut-oil-and-alzheimer%e2%80%99s-disease/
http://www.coconutketones.com/


Coconut Oil and Alzheimer’s Disease
October 5, 2010

How worried should drug companies be about supplements eating into their monopoly profits? A lot—as this story will show. Please share it with anyone you know who is suffering from Alzheimer’s or is worried about it.

Of course, just about everyone worries about Alzheimer’s. It currently afflicts 5.2 million people in the US and is the seventh leading cause of death. The cost of treating it is estimated at $148 billion.

Mary Newport, MD, has been medical director of the neonatal intensive care unit at Spring Hill Regional Hospital in Florida since it opened in 2003. About the same time the unit opened, her husband Steve, then 53, began showing signs of progressive dementia, later diagnosed as Alzheimer’s Disease. “Many days, often for several days in a row, he was in a fog; couldn’t find a spoon or remember how to get water out of the refrigerator,” she said.

They started him on Alzheimer’s drugs—Aricept, Namenda, Exelon—but his disease worsened steadily. (It should be noted that the latest research shows that the various Alzheimer’s drugs, like Aricept, have proven disappointing, with little real benefit and often distressing side effects.) When Dr. Newport couldn’t get her husband into a drug trial for a new Alzheimer’s medication, she started researching the mechanism behind Alzheimer’s.

She discovered that with Alzheimer’s disease, certain brain cells may have difficulty utilizing glucose (made from the carbohydrates we eat), the brain’s principal source of energy. Without fuel, these precious neurons may begin to die. There is an alternative energy source for brain cells—fats known as ketones. If deprived of carbohydrates, the body produces ketones naturally.

But this is the hard way to do it—who wants to cut carbohydrates out of the diet completely? Another way to produce ketones is by consuming oils that have medium-chain triglycerides. When MCT oil is digested, the liver converts it into ketones. In the first few weeks of life, ketones provide about 25 percent of the energy newborn babies need to survive.

Dr. Newport learned that the ingredient in the drug trial which was showing so much promise was simply MCT oil derived from coconut oil or palm kernel oil, and that a dose of 20 grams (about 20 ml or 4 teaspoons) was used to produce these results. When MCT oil is metabolized, the ketones which the body creates may, according to the latest research, not only protect against the incidence of Alzheimer’s, but may actually reverse it. Moreover, this is also a potential treatment for Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease), drug-resistant epilepsy, brittle type I diabetes, and type II (insulin-resistant) diabetes.

So Mr. Newport, not being able to get into the drug trial, started taking the coconut oil twice a day. At this point, he could barely remember how to draw a clock. Two weeks after adding coconut oil to his diet, his drawing improved. After 37 days, Steve’s drawing gained even more clarity. The oil seemed to “lift the fog,” and in the first sixty days, Dr. Newport saw remarkable changes in him: every morning he was alert and happy, talkative, making jokes. His gait was “still a little weird,” but his tremor was no longer very noticeable. He was able to concentrate on things that he wanted to do around the house and in the yard and stay on task, whereas before coconut oil he was easily distractible and rarely accomplished anything unless he was directly supervised.

Over the next year, the dementia continued to reverse itself: he is able to run again, his reading comprehension has improved dramatically, and his short-term memory is improving—he often brings up events that happened days to weeks earlier and relays telephone conversations with accurate detail. A recent MRI shows that the brain atrophy has been completely halted.

Let’s take a moment to consider what actually happened here. Synthetic (patentable) Alzheimer’s drugs have failed. A drug company reluctantly decides to put a non-patentable natural substance (medium-chain triglycerides derived from coconut or palm) through an FDA trial. It works. But, darn it, a smart doctor figures out that a natural food can be substituted for the super-expensive drug. Not only that, the ketones from natural coconut oil last in the body longer than the drug version—eight hours instead of three hours. This is enough to make a drug company start worrying about its future. What if this natural health idea really catches on? Goodbye to monopoly profits!

Coconut oil can be found in many health food stores and even some grocery stores. One large chain sells a non-hydrogenated (no trans-fat) brand of coconut oil in a one-liter size (nearly 32 ounces) for about $7. It can be purchased in quantities as small as a pint and up to five gallons online. It is important to use coconut oil that is non-hydrogenated and contains no trans-fat. We would also strongly encourage the use of virgin oil (chemicals used to extract non-virgin oil are potentially dangerous, and better still, virgin organic, still quite reasonably priced.)

For more information, see Dr. Newport’s website. Sadly, you will not find any information on ketones, or the use of coconut oil or MCT oil, on the Alzheimer’s Association website.

Coconut oil is not the only natural product that has the potential to turn Alzheimer’s around. We will cover some other ones, and drug industry efforts to steal some of them, in a future issue.

Synapsin
10-19-2010, 07:57 AM
Nothing new per say but still a good paper.

Barn01
10-27-2010, 05:19 PM
Better late than never but Sorry for your loss No Hype :(

Just to add to this discussion I found this article about how just walking can improve the condition. (not sure if repost)

http://www.naturalnews.com/030180_walking_Alzheimers.html

NO HYPE
10-27-2010, 05:42 PM
Better late than never but Sorry for your loss No Hype :(

Thank you. Still struggling with his loss.




Just to add to this discussion I found this article about how just walking can improve the condition. (not sure if repost)

http://www.naturalnews.com/030180_walking_Alzheimers.html

Exercising combined with a nutraceutical approach is extremely beneficial [even more so in the years prior to a diagnosis]. I wish my dad could have had the oppertunity to walk/exercise properly following his diagnosis. Thanks again.

robertmm94
12-06-2010, 08:08 PM
i know this is late, but i am immensely sorry for your loss, Dementia is a very hard disease to deal with and i envy you for coming up with your supplementation protocol to help your father live a higher quality of life with the disease he was given. My grandmother passed away from dementia about 2 years ago and this thread is really opening my eyes to advising my father to take some of these nutrients. Its actually the first supplement related protocol he is listening to me on(he is very stubborn in taking anything).
i would love to to know your opinion on this supplementing/ dosing protocol, and it would mean a lot to me and in my mind would greatly help my father.

so far on my life i have.

curcumin (500 mg x2 a day)
NOW Virgin Coconut Oil ( 1g x 3 a day)
vitamin c (2-3 grams a day spread out in 500 mg dosages)
Now NAC (600 mg x 1(?)2 daily, with vitamin c )
Nature's Science Vitamin B-Complex( 1[?]2 a day )
vitamin D(2000 UI x 2 a day)
Dha( gram of dha , 500 morn, 500 night)
Higher Power R-ALA (200mg x 3 day)
NOW Choline & Inositol(250mg each x3 a day)
grape seed (100x 2-3 a day)

also was thinking of adding green tea, huperzine a and gingko?these worth it?


im assuming my dad with not want to take all of these. would you recommend taking any out or putting any in? along with any dosage changes? thanks so much for your time man.

on a side note. my mother is going into surgery for hip replacement and hoping some of these anti oxidants will add in recovery.

NO HYPE
12-07-2010, 09:04 AM
Higher Power R-ALA

I'd drop that one due to poor bioavailability. Go with Na-RALA.




NOW Choline & Inositol

I'd drop that one for a better source of choline --> CDP choline, phosphatidylcholine, phosphatidylserine, ALCAR, taurine [NOTE: disreguard the ALA/glutamine content] http://www.bodybuilding.com/store/jarrow/neuro-optimizer.html



grape seed

I would drop the grape seed for ubiquinol: http://www.bodybuilding.com/store/now/ubiq.html




vitamin D (2000 UI x 2 a day)

You need vitamin D3 [cholecalciferol].




also was thinking of adding green tea, huperzine a and gingko?these worth it?

I would just go with what you've listed for now.




on a side note. my mother is going into surgery for hip replacement and hoping some of these anti oxidants will add in recovery.

Indeed [to what extent I am not sure however, the aforementioned protocol will ameliorate symptom severity to some degree]. I would seek the use of high-dosed glutamine. Additionally, I have heard many great things about Super Cissus RX and speeded recovery from surgery/bone healing.

robertmm94
12-07-2010, 07:50 PM
I'd drop that one due to poor bioavailability. Go with Na-RALA.





I'd drop that one for a better source of choline --> CDP choline, phosphatidylcholine, phosphatidylserine, ALCAR, taurine [NOTE: disreguard the ALA/glutamine content] http://www.bodybuilding.com/store/jarrow/neuro-optimizer.html




I would drop the grape seed for ubiquinol: http://www.bodybuilding.com/store/now/ubiq.html





You need vitamin D3 [cholecalciferol].





I would just go with what you've listed for now.





Indeed [to what extent I am not sure however, the aforementioned protocol will ameliorate symptom severity to some degree]. I would seek the use of high-dosed glutamine. Additionally, I have heard many great things about Super Cissus RX and speeded recovery from surgery/bone healing.

thank you, sounds good. and high dosed glutamine? for what reason? and yes i was thinking about getting her super cissus rx for that reason .

also would you dose b vitamin at 1 or 2 a day? also nac? also im assuming i i would give nac with vitamin c unless there was going to be an inflammatory response in the near future ?

robertmm94
12-08-2010, 08:03 PM
I'd drop that one due to poor bioavailability. Go with Na-RALA.





I'd drop that one for a better source of choline --> CDP choline, phosphatidylcholine, phosphatidylserine, ALCAR, taurine [NOTE: disreguard the ALA/glutamine content] http://www.bodybuilding.com/store/jarrow/neuro-optimizer.html




I would drop the grape seed for ubiquinol: http://www.bodybuilding.com/store/now/ubiq.html





You need vitamin D3 [cholecalciferol].





I would just go with what you've listed for now.





Indeed [to what extent I am not sure however, the aforementioned protocol will ameliorate symptom severity to some degree]. I would seek the use of high-dosed glutamine. Additionally, I have heard many great things about Super Cissus RX and speeded recovery from surgery/bone healing.

thank you for all the help. how would you dose ubiquinol ?

DR_P
12-09-2010, 04:18 AM
thank you, sounds good. and high dosed glutamine? for what reason?

high dosed glutamine and dementia? that calls for an explanation.

NO HYPE
12-10-2010, 03:33 PM
high dosed glutamine and dementia? that calls for an explanation.

Sorry, the aforementioned comments sidetracked the original discussion. Total hip replacement has been used clinically as a reproducible trauma model. Post-surgey nonessential amino acids in muscle commonly decline however, glutamine is subjected to more significant decrements than any other amino acid. High-dosed glutamine following "hip replacement" in an effort to....

[1] Ameliorate significant decrements in plasma/intramuscular glutamine concentrations post-surgery [40% lower than in healthy volunteers].

[2] Attenuation of skeletal muscle catabolism.

[3] Maintainence of skeletal muscle protein synthesis.

[4] Enhancement of whole-body nitrogen balance.

[5] Enhancemnet of HLA-DR expression

[6] To ameliorate depression of the overall immune response.

On Fire
12-11-2010, 03:16 PM
Great thread... I'll have to reread this one later. I've lost two grandparents to alzheimers, and I would definitely like to know how to better deal with it (lessen it) in the future...

labradarep
12-11-2010, 06:15 PM
Surprised no green tea extract here... some great nutrients though.
I think a potent Boswellia extract would go well here to deal with the 5-lipooxygenase pathway of inflammation. Lyprinol is supposedly amazing too.
http://www.aor.ca/int/related_research/maxi-boz.php

What about aspirin, even a 81mg daily dose may help with the low dose reducing risk of problems.

And about the iron. It can be especially a problem for men and that is why donating blood is great for men in reducing a build up of iron...

One of the studies you posted on iron talked about the potential of iron chelators... one of or the best found in nature IP6 has an indirect antioxidant effect through it's chelation of free iron, preventing the formation of damaging hydroxyl radicals. It also chelates other minerals, manganese likely too.
http://www.aor.ca/int/related_research/ip6.php

As you can see AOR provides many answers in the quest for longevity and disease prevention. Great company and very professional/science based.
Their Ortho Core multi provides many of the ingredients needed for optimum health. I take 1-2 with every meal.

Hope you got something out of my post anyways.

Lyprinol works extremely well on my mother who has arthritis. She only uses half the recommended dose each day & see's quite dramatic result.

Funny how I have not seen Phosphatidyl Serine , Bacopa or Vinpocetine mentioned.

I would think that PS would be very effective???

Great Thread BTW. Thanks to all who have contributed.

robertmm94
12-16-2010, 04:18 PM
Sorry, the aforementioned comments sidetracked the original discussion. Total hip replacement has been used clinically as a reproducible trauma model. Post-surgey nonessential amino acids in muscle commonly decline however, glutamine is subjected to more significant decrements than any other amino acid. High-dosed glutamine following "hip replacement" in an effort to....

[1] Ameliorate significant decrements in plasma/intramuscular glutamine concentrations post-surgery [40% lower than in healthy volunteers].

[2] Attenuation of skeletal muscle catabolism.

[3] Maintainence of skeletal muscle protein synthesis.

[4] Enhancement of whole-body nitrogen balance.

[5] Enhancemnet of HLA-DR expression

[6] To ameliorate depression of the overall immune response.

Thank you for all the help. My moms surgury is tomorrow and was just wondering what is an ideal dose ? Would high dose be 20g day spread out? Sorry to stray from original topic .

Marcus8880
12-17-2010, 07:53 AM
How about any dietary changes? Look into a paleo diet where there is absolutly no grains to inflame the body. I pretty much cured my ****tis and chronic health problems with it.

bloodsimple1234
12-17-2010, 03:16 PM
How about any dietary changes? Look into a paleo diet where there is absolutly no grains to inflame the body. I pretty much cured my ****tis and chronic health problems with it.

grains are not an issue,many have omega 3's not just 6.

grains,when taken with fiber are good for you.

supernoober
12-22-2010, 05:37 PM
I tried messaging you but your mailbox is full. You seem very knowledgeable about biological processes and physiology. I'd appreciate any information regarding the following:

What multi-vitamin do you take?

Do you think quercetin is good to dose daily (in multi-vitamin complex)?

Would you recommend milk-thistle/NAC prior to and after alcohol consumption?

Would milk thistle or NAC help with acne (by helping the liver)?

would the amounts of antioxidants in multi vitamins such as activite sport, orange triad, or source naturals life force negate bodybuilding gains if taken close to work out?

Do you know anything about kre-alkalyn?

Do you take any drugs, recreational or prescription?

Do you think there are any long term negative effects from taking Triazole?
http://www.bodybuilding.com/store/drivensports/triazole.html

Thanks

Peter LeDrew
12-22-2010, 08:12 PM
Lyprinol works extremely well on my mother who has arthritis. She only uses half the recommended dose each day & see's quite dramatic result.

Funny how I have not seen Phosphatidyl Serine , Bacopa or Vinpocetine mentioned.

I would think that PS would be very effective???

Great Thread BTW. Thanks to all who have contributed.


There`s dozens of possibly great ingredients so some will always go unmentioned. Phosphatidyl Serine or PS has some great research and is an expensive one as well. I get 75mg from each serving of Ultima. I also get vinpocetine and Bacopa from AOR`s Ortho Mind.

Great to hear real feedback on Lyprinol. It seems like one of the best anti-inflammatory ingredients around.


How about any dietary changes? Look into a paleo diet where there is absolutly no grains to inflame the body. I pretty much cured my ****tis and chronic health problems with it.


grains are not an issue,many have omega 3's not just 6.

grains,when taken with fiber are good for you.


For some people with real gluten intolerance or allergies, avoidance of gluten rich foods such as some grains can be a life saver. Gluten can trigger a nasty inflammatory cascade in such people causing the chronic health issues you mention like ****tis.

CALLofDUTY
12-26-2010, 10:37 PM
Sorry for your loss, stay strong brother. You are a very valuable member to these boards.

papagunz
12-27-2010, 08:07 AM
grains are not an issue,many have omega 3's not just 6.

grains,when taken with fiber are good for you.

A little strong wording there homez. Some people really do get inflammation from grains. It's akin to lactose intolerance. Evolutionarily some populations got around it (ie: lactase remaining 'on' into adulthood in pastoral cultures) Others don't get quite so lucky.

Edit: We do agree on the fatty acids issue however. Domestication served to be a negative as corn fed beef stuck in a box until death don't have the quality efa profile of free range beef.

SevenTH
02-05-2011, 11:11 AM
Hello all of you , i read over and over this amazing thread and big thanks for NO HYPE,although so sad and sorry for your lose - i'm on the edge of experiencing the same : my mother.Long story short,she was diagnosticated 3 years ago at 61yo, with AD,started on Exelon by neurologist and now( about 1 year ) she's on Memantine,Aricept,Tanakan and Cipralex, but despite of this heavy medication ,her mental state degrades fast as never expected .Maybe it's late,but we try to don't give up,so i have the following stack,for which i would ask you what could be a good timing for a day :

NAC - already in the morning before breakfast
B-Right , Methylcobalamin 1000mcg,DHA 500mg,Citi****ne,D3 2000UI, Curcumin C3 .
From this point i'm not aware which parts of the day I should give her the aforementioned supplements and some advice will be wellcomed.

MJ1331
02-05-2011, 01:52 PM
Hello all of you , i read over and over this amazing thread and big thanks for NO HYPE,although so sad and sorry for your lose - i'm on the edge of experiencing the same : my mother.Long story short,she was diagnosticated 3 years ago at 61yo, with AD,started on Exelon by neurologist and now( about 1 year ) she's on Memantine,Aricept,Tanakan and Cipralex, but despite of this heavy medication ,her mental state degrades fast as never expected .Maybe it's late,but we try to don't give up,so i have the following stack,for which i would ask you what could be a good timing for a day :

NAC - already in the morning before breakfast
B-Right , Methylcobalamin 1000mcg,DHA 500mg,Citi****ne,D3 2000UI, Curcumin C3 .
From this point i'm not aware which parts of the day I should give her the aforementioned supplements and some advice will be wellcomed.

Im in the same boat with my grandmother. She has advanced Alzheimer's disease. I wish there was an effective treatment but unfortunately the effects of Rx's and supplements are marginal at best. Build up of Tao proteins are one of the major problems of Alzheimer's which leads to inflammation and other disease processes. As much as i wish supplements would help, it is very unlikely it would help with the true cause.

However, If anyone has any anecdotal stories im quite interested in them.

NO HYPE
02-08-2011, 10:37 AM
Im in the same boat with my grandmother. She has advanced Alzheimer's disease. I wish there was an effective treatment but unfortunately the effects of Rx's and supplements are marginal at best. Build up of Tao proteins are one of the major problems of Alzheimer's which leads to inflammation and other disease processes. As much as i wish supplements would help, it is very unlikely it would help with the true cause. However, If anyone has any anecdotal stories im quite interested in them.

I think people are often times too quick in disreguarding the nutraceutical approach. TNF-alpha & NF-kB are of the same signal transduction pathway, and both relate to the etiology of AD [as well as a number of other diseases]. In terms of AD, you might want to start by taking a look at the nutraceutical data pertaining to the suppression of excessive NF-kB signaling/phosphorylation [and the accompanying inflammatory/neurodegenerative response that follows]. Likewise, the inhibition of TNF-alpha/lipopolysaccaride-induced neuronal tau phosphorylation in neuronal cell lines. As an example, you might want to look into curcumin, D3, & DLPC [dilinoleoylphosphatidylcholine]. Epidemiological studies have indicated that curcumin can significantly reduced the risk of Alzheimer's disease. Additionally, I believe Curcumin has demonstrated it's ability to stimulate immune clearance of amyloidosis via the modulation of beta-amyloid precursor protein metabolism. Below is merely a brief list of the literature in which I am referring to.


Donald Yance
Cancer and Inflammation: The emerging role of botanical compounds in targeting proinflammatory pathways, with particular attention to the NF-kB signaling pathway

Eukaron, Vol. 1, 4-5, January 2005
Arun George Paul
NF-kB A Novel Therapeutic Target for Cancer

Journal of Cancer Molecules 4(1): 11-16, 2008.
Chih-Li Lin and Jen-Kun Lin
Curcumin: a Potential Cancer Chemopreventive Agent through Suppressing NF-kB Signaling

Neuroscience. 2009 Dec 29;164(4):1744-53. Epub 2009 Sep 27.
Pandey NR, Sultan K, Twomey E, Sparks DL.
Phospholipids block nuclear factor-kappa B and tau phosphorylation and inhibit amyloid-beta secretion in human neuroblastoma cells.

Biochem Biophys Res Commun. 2002 Jun 21;294(4):849-53.
Cao Q, Mak KM, Lieber CS.
Dilinoleoylphosphatidylcholine decreases LPS-induced TNF-alpha generation in Kupffer cells of ethanol-fed rats: respective roles of MAPKs and NF-kappaB.

NO HYPE
02-08-2011, 11:41 AM
My mother. Long story short, she was diagnosed 3 years ago at 61yo, with AD, started on Exelon by neurologist and now (about 1 year) she's on Memantine, Aricept, Tanakan and Cipralex, but despite of this heavy medication, her mental state degrades fast as never expected. Maybe it's late, but we try to refrain from giving up, so i have the following stack, for which i would ask you what would be the best way to approach timing the doses?

NAC - already in the morning before breakfast
B-Right, Methylcobalamin 1000mcg, DHA 500mg, Citi****ne, D3 2000 UI, Curcumin C3.

From this point i'm not aware which parts of the day I should give her the aforementioned supplements and some advice will be wellcomed.

Honestly, I feel it's best to maintain an even balance when it comes to dosing protocols. I'd try to spread them evenly throughout the day. I'd also consider adding vitamin C, dilinoleoylphosphatidylcholine, and SAMe [as well as some of the other nutraceuticals previously mentioned]. Nonetheless, I would not expect to see any significant results at such a late stage in the disease. Either way, I feel it's a great approach to lessening the chances of developing such a terrible affliction. Good luck.

papagunz
02-09-2011, 10:10 AM
Epidemiological studies have indicated that curcumin can significantly reduced the risk of Alzheimer's disease. Additionally, I believe Curcumin has demonstrated it's ability to stimulate immune clearance of amyloidosis via the modulation of beta-amyloid precursor protein metabolism. Below is merely a brief list of the literature in which I am referring to.

I read a very interesting study where D3 (downstream metabolites) and curcumin work additively in type 1 macrophages to induce AB phagocytosis as well! Pretty damn cool.

http://www.ncbi.nlm.nih.gov/pubmed/19433889
http://www.ncbi.nlm.nih.gov/pubmed/16988474

NO HYPE
02-09-2011, 11:55 AM
I read a very interesting study where D3 (downstream metabolites) and curcumin work additively in type 1 macrophages to induce AB phagocytosis as well! Pretty damn cool.

http://www.ncbi.nlm.nih.gov/pubmed/19433889
http://www.ncbi.nlm.nih.gov/pubmed/16988474

Thank you. I forgot to cite those.

SevenTH
02-10-2011, 07:27 AM
Thank you NO HYPE, I am grateful for your advices . Regarding to your guidance,I'm assuming that it might be a connection between an improper liver activity and neurological function , DLPC together with SAMe being involved in the anti-inflammatory process and TNF-alpha attenuation, bile flow and cholesterol enrichment . My mother constantly used to deal with hepatic issues due to a lazy bile .
Worst concern is about her evolutional lack of speech , beginning couple of years ago with being less talkative, repetitive words and becoming almost speechless in last months .She can only repeat some words if we tell her over and over .
The only thing that seems it worked it was ALCAR, with a daily charge of 2 g , spreaded throughout a day , but no more noticeable improving .
I'm not very sure , but could be dilinoleoylphosphatidylcholine to be found in essentiale forte made by Sanofi ?

NO HYPE
02-10-2011, 10:16 AM
My mother constantly used to deal with hepatic issues due to lazy bile.


I reviewed some rather positive results pertaining to the downregulation of degenerative decline/neuronal apoptosis, via the administration of TUDCA [i.e. RM Ramalho et al, 2008 - Bile acids and apoptosis modulation: an emerging role in experimental Alzheimer's disease]. It looks like LiverLonger may aquire some benefits that we were not previously aware of.

ROS-mediated ATP dysfunction results in canalicular bile salt export pump impairment, thereby worsening the severity of intrahepatic cholestasis. So while directly treating bile flow via TUDCA and/or polyenephosphatidylcholine (PPC) is a VERY wise and efficient choice.... the attenuation of ROS-mediated damage via NAC, SAMe and/or Na-RALA is equally as important.




Worst concern is about her evolutional lack of speech , beginning couple of years ago with being less talkative, repetitive words and becoming almost speechless in last months. She can only repeat some words if we tell her over and over.

I know what you are going through, and you have my sympathy. Watching a once strong-minded individual who had such a significant impact in your life, slowly regress into a mental state reflecting that of an infant, was the hardest thing in life that I've had to deal with thus far.




I'm not very sure, but could dilinoleoylphosphatidylcholine be found in essentiale forte made by Sanofi ?

I would suggest looking into a quality lecithin product. PPC [polyenylphosphatidylcholine] is a mixture of phosphatidylcholines [primarily PCPC & DLPC].

http://www.bodybuilding.com/store/now/lecithin.html

~

NO HYPE
02-10-2011, 10:30 AM
^^ aspirin ^^ :(

Cerebral microbleeds have been linked with cerebral amyloid angiopathy, a condition in which amyloid-beta forms vascular deposits, leading to AD. A study from the June 2009 issue of the Archives of Neurology focused on the cerebral impact of antithrombotic drugs in elderly patients and found that the salicylate fraction of aspirin was linked to a higher prevalence of micro-lobar bleeds when compared to patients using carbasalate calcium.

Arch Neurol. 2009 Jun;66(6):714-20. Epub 2009 Apr 13.
Vernooij MW, Haag MD, van der Lugt A, Hofman A, Krestin GP, Stricker BH, Breteler MM.
Use of antithrombotic drugs and the presence of cerebral microbleeds: the Rotterdam Scan Study.

BobisMighty
02-10-2011, 01:42 PM
Do you think these supplements would work with other inflammatory diseases such as MS?

NO HYPE
02-10-2011, 04:33 PM
Do you think these supplements would work with other inflammatory diseases

Some of them, yes. While I won't really get into the myriad of diseases that relate to this topic [one must first take a close look at the etiology of each disease], the pathophysiology of inflammatory disease basically stems from mutated/excessive NF-kB signaling/phosphorylation, and often includes mutated TNF-a/IL-1 expression [to explain it briefly].

SevenTH
02-12-2011, 01:43 PM
I would suggest looking into a quality lecithin product. PPC [polyenylphosphatidylcholine] is a mixture of phosphatidylcholines [primarily PCPC & DLPC].

Now Lecithin Triple Strength

~

Thank you kindly . Speaking about TUDCA, I recall you stated about benefits in previous pages, but I have an hesitation between choosing LiverLonger (as you recommended ) or Ursofalk which actually is UDCA , last one have the same concentration of 250mg .

I have already SAMe 200mg form, but the tragic irony is the expire date which was OCT 2010 .However, I kept it in the fridge and I was wondering if would be this still usable ? I'm asking because many drugs manufacturers still grant for the term of validity for another 6 months .

NO HYPE
02-12-2011, 03:34 PM
Speaking about TUDCA, I recall you stated about benefits in previous pages, but I have an hesitation between choosing LiverLonger (as you recommended ) or Ursofalk which actually is UDCA

My vote goes to tauroursodeoxycholic acid --> LiverLonger.




I have already SAMe 200mg form, but the tragic irony is the expire date which was OCT 2010. However, I kept it in the fridge and I was wondering if would be this still usable?

I doubt there has been much time-induced degradation of the product. More importantly however, is the SAMe enterically-encapsulated? If not, find a new manufacturer.

SevenTH
02-13-2011, 09:04 AM
That SAMe is a Jarrow enteric coated packed in foil blister and a big concern would be the warning for an already administration of SSRI and MAO inhibitors such as my mother is on Cipralex .

Timing the doses of supplements :
Before breakfast :
NAC 600 x 1
Vitamin C 200mg x 1
B-Right x 1
MethylB12 1000mcg x1 crumbled and diluted in few water drops and then intranasally applied
CDP Choline 250mg x 1
After breakfast :
1 tsp coconut oil ( gradually increasing to 1 tbsp)
Now DHA 500 x 1
In the evening, after dinner :
1 tsp coconut oil ( gradually increasing to 1 tbsp)
Now DHA 500 x 1
D3 2000UI x 1
Curcumin C3 500mg x 1 ( gradually increasing to 2g )

I'll start her also with silymarin 3 times a day.Her prescribed medication consist in memantine(Ebixa), Cipralex in the morning, Aricept,memantine in the evening along with Tanakan 3 times a day.Therefore would be fine to introduce SAMe in the evening (as possible apart from Cipralex) ? Neurologist insisted to get Cipralex for anxiety and social disorder.

Surive123
02-21-2011, 04:15 PM
Thoughts on this?

http://www.ncbi.nlm.nih.gov/pubmed/17153958


Emoxypine, thiotriazoline, and NN-103 (a 4-hydrazinoquinasoline derivative) exhibit a pronounced neuroprotective action during acute cerebral stroke. Emoxypine and thiotriazoline are more effective in inhibiting death of neurons in the sensomotor area of the frontal cortex, while NN-103 is more active in the hippocampus. The ischemic death of neurons in the sensomotors area of the frontal cortex with equal probability takes place by karyopyknosis or cytolysis, while in the hippocampus, mainly by cytolysis. All preparations (except for piracetam) with antioxidants properties are powerful membranoprotective agents, which is confirmed by a considerable decrease in the rate of cytolysis both in the cortex and in the hippocampus. The use of piracetam in the case of acute cerebral stroke increases the rate of neuronal death in various areas of the cortex, up to complete destruction of nerve tissues with the formation of cysts (in hippocampus). The tested preparations exhibit different mechanism of neuroprotection: emoxypine and NN-103 (in the sensomotor area of the frontal cortex and hippocampus) and thiotriazoline (in the hippocampus) produce the neuroprotection action on the background of increased activity of transmissions and transcription processes, while thiotriazoline (in the sensomotor area of the frontal cortex) offers neuroprotection on the background of inhibited transcription and transmission activity.



There is some suggestion (but no statistically significant result) of an unfavourable effect of piracetam on early death, but this may have been caused by baseline differences in stroke severity in the trials. There is not enough evidence to assess the effect of piracetam on dependency

http://www.ncbi.nlm.nih.gov/pubmed/16625535