1230 replies to this topic

[Anthony]

Thanks for posting this article. I must have missed it when reading through Google News this morning.

Edited by Michael, 23 February 2012 - 03:05 PM.

[Lauren]

Hey Everyone,

My apologies for not having prefaced my interjections here by introducing myself, but I just find this all to be very fascinating and deeply engaging. It has utterly piqued my interest as one whom, I must confess, knows very little about the physiochemical underpinnings of systems, whether they manifest themselves biochemically or not (well, upon a second reflection, it seems that most things are biologic unless they occupy the realm of physics and mechanisms on the level of quanta, but I would imagine - and being a novice to this particular field I can only speculate - that these very quantum mechanical interactions contribute to an extent to the overall ontogeny of biomechanics. I see quantum electrodynamics as being on a very esoteric micro-systemic level which we cannot penetrate just yet. And I wish that I were not so addled by the degenerative effects of aging on the mind. I am and feel like I have already lived three quarters of my life, and I've not yet finished past 30. So this is why I am so interested in the intrigue behind SENS theory. Now as in all things scientific, I do not profess to be an expert, but I do have an epistemological and gestalt understanding of how various systems work, in that I can perceive of their relative synergistic properties and interpolate (or extrapolate, depending upon how much I know about a given system and its complementary system. It is a general axiom in the analysis of scientific systems that you cannot extrapolate the properties of one system to a completely different system, as not all systems are compatible. This is true with all things). But I would have to admit to the fact that this is all a relatively unfamiliar territory not only for myself, but for most of science. Much if it is still inherently speculative. It is conceivable though, and it seems to be situated just after the horizon of scientific discovery. I believe that there is such a thing as a Kurzweilian singularity whereby Artificial Intelligence will allow us to literally reprogram the human genome, but even at this current stage it has very much achieved a sort of nascent incipiency. We have come a long way since the making of the atomic bomb, but the pace of scientific discovery to my mind is surely not fast enough to be concordant with Kurzweilian theory. But the process has largely been expedited within the last quarter of a century (and will only continue to grow, so long as we utilize our technologies for progressive means such as toward the development of more efficacious methodologies in the fields of medicine and biochemical engineering alike).

But I am not certain that, as you had pointed out, you can override some of these metabolic systems, and I worry that the pharmaceutical companies may very much be synthesizing drugs that could have iatrogenic consequences for their patients. I think that the field of biochemical engineering needs to codify a better way of synthesizing these drugs. It would be a huge advantage if biochemists could somehow create better synthetic agonists which mimic neurotransmitter binding at receptor sites. But I think that surely all these developments incur a risk. However, there is a fundamental error in incorporating the deontological view of saying that in certain scenarios, if the consequences of incurring these risks transpire in isolated incidences of iatrogenic effects experienced by mere clusters of a few patients, then this could merely just be dismissed as a rare side effect, and therefore all the FDA has to do is put warning labels on medications. Well, I do not think that this is sufficient enough. There is no compensatory equivocation which would reconcile the cost of one life to the overall pursuit of the pharmaceutical industries, and losing one life due to iatrogenic side-effects is ultimately not worth all the money being put into the biochemical synthesis of these drugs; and more importantly it is even more devastating for the patient who spent millions of dollars on drugs to experience fatal side-effects. It just doesn't add up.....If anything, I think that what the pharmaceutical companies are doing to people these days is not only unethical, but also inhumane. I just think that there needs to be far more oversight in the development of these meds. There have to be a LOT more restrictions placed on the development of such drugs, and on the tests. In fact, as soon as there is any anomaly, biochemical engineers should be able to fix it.

So the crux of my argument here is that there has to be some alternative way of engineering these medications besides doing so synthetically. I think that the one thing which would rescue the human genome would be genetic engineering. But we have to incorporate the uses of the allosteric regulations in transcriptase enzymes which code for such proteins. So all these little intricate parts need to be reassembled through genetic engineering, and in order to go about doing this, we really need to look on the level of enzymatic interactions involved in the allosteric regulation of protein synthesis, which creates the amino acid sequences that comprise DNA. We also need to ascertain how these interactions apply to the entire system as a whole. In order to actualize the singularity of our scientific potential, we need to abandon the idea of merely synthesizing agonists that mimic other neurotransmitters, as this is an extrapolative, macrostructural approach. We have to look on the molecular level of protein synthesis, and then build up from there

I also think that there's been some confusion on one particular point:

No confusion. Brain function was improved by targetting BDNF irrespective of deposit level. If I am predisposed to, or experiencing the affects of Alzheimers, I'd like to halt its progression and reverse its affects rather than lose my memories. If the gunk building up can be removed as well, super.

Moreover, as Aubrey regularly emphasizes, dynamic metabolic pathways like the ones regulating BDNF are 'set' where they are for a reason, and overriding those regulatory pathways inevitably carries risks; in the case of boosting BDNF, the most obvious one would be cancer, since many cancers (including, in particular, neuroblastomas in the brain) exploit the BDNF signaling pathway to help them resist apoptotic signaling and increase needed vascularization:

But of course. Any intervention carries risks. Even those that simply try to degrade aggregates. We currently have a plethora of drugs that alter various metabolic and regulatory pathways directly or indirectly today. What's a few more?

On that first bit, (a) the fact that BDNF is effective "independent of the amount of amyloid deposited" isn't evidence that Abeta isn't a major contributor to AD, or that its removal isn't central to its arrest and ultimate reversal; rather, it's again evidence for what has actually been the dominant model for much of the last decade: that the smaller, soluble oligomeric Abeta species, rather than the deposited, fibrillar plaque, is the critical Abeta species (though the plaque is unlikely to be helpful except as a dispensible 'sink'). Similarly on the alpha-secretase experiment:

With Alzheimer's, has there been any evidence that the accumulating junk is anything beyond a useful biomarker, i.e. actually impacting memory and cognition? I have yet to see any. This phase I trial cleared amyloid plaques but the progression of the disease continued!

Although immunisation with Abeta(42) resulted in clearance of amyloid plaques in patients with Alzheimer's disease, this clearance did not prevent progressive neurodegeneration.

Link: http://www.ncbi.nlm....pubmed/18640458

But I think that the idea that an agent to protect cells from the toxic effects of aging damage is ultimately superior to repairing that damage is somewhat implausible on its face: certainly, BDNF might be a good short-term, stopgap measure, but it can only reduce the damaging effects, not eliminate them, whereas removing the underlying damage removes the secondary effects of that damage gratis.

Organisms and their cells already have agents to protect themselves from toxicity for numerous decades. If there are mechanisms already in place(immune system, microglia and other macrophages, organelles, dna repair, etc) that can protect against aging and finding a means to prop them up might be a better alternative than simply trying to mop up all the "after the fact" downstream damage. This would be true particularly if numerous innate repair mechanisms are declining with time. The "ounce of prevention is worth a pound of cure" approach may be our fastest route to significant longevity. I'm all for targeting after-the-fact damage but I don't see any data yet that suggests that cleaning it up is going to have all that significant of an impact on longevity, it's just speculation at this point, as is any other theoretical approach.

As to (b) the op cit comments of Drs. Mufson and Koliatsos: this is in my view hyperbolic at best. In particular, to say that the new study "comes at a time when amyloid, the predominant target of therapy for Alzheimer disease, has not given us great therapeutic products or solutions" is really not very helpful...

I don't disagree that slamming existing efforts is helpful but I don't follow your subsequent line of reasoning. It suggests that there is only one solution to the problem and we simply need to give targeting the aggregates more time, which I am all in favor of. I'm not a fan of ruling out any proposal, particularly for diseases we still know so little about. Are you suggesting that all researchers should focus on a single strategy to deal with Alzheimer's? I wouldn't want to put all my eggs in one basket. Studying the regulatory mechanisms, metabolic changes and existent repair mechanisms could and likely will lead to a much more effective treatments.

[mentatpsi]

there's a show right now on HBO called The Alzheimer Project. It's pretty interesting.

[Mind]

Protein inhibitor helps rid brain of toxic tau protein

Glad to see more and more researchers thinking about age related diseases as multi-factorial problems and getting beyond the "find the single silver bullet" approach.

The USF researchers originally thought activating Hsp70 would direct the chaperone protein to decrease the tau gone bad -- preventing tau from stacking up into tangles inside cells involved in memory and destroying them. But instead of restoring tau to its normal supportive function, activating Hsp70 actually led to tau's preservation and even more accumulation, Dickey said. "Basically we think the chaperone binds to the tau, and somehow in the process of trying to fix things decides to keep holding onto tau when it shouldn't. So, activating Hsp70 is not necessarily what we want to do; we ultimately want to inhibit Hsp70 to promote the release or clearance of tau …to kill the bad tau."

Dr. Dickey emphasizes that problems with Hsp70 alone do not cause Alzheimer's. It likely develops from a convergence of various factors in the brain, he said, including deposits of the other featured Alzheimer's protein beta amyloid, or a genetic defect; disruption of cell signaling; a breakdown in the neuron's support structure, and then accumulation of tau into the memory-choking tangles.

[tunt01]

http://www.scienceda...91022114315.htm

seems to dovetail nicely with the ongoing discussions of methylene blue and the 'death' of the AB hypothesis about alzheimer's.

- scientists improve AB clearance by increasing IL-6, which stimulates removal by microglial.

the amyloid plaques were removed from the brain. Their analysis revealed that the inflammation induced by IL-6 in the brain directed the microglia cells to remove the amyloid plaques from the brain. Microglial cells do this by phagocytosis. "They gobble up the plaque, which they 'see' as a foreign invader, and break it apart," Dr. Das says. Researchers also found that activated microglia cells were closely attached to the plaques and expressed proteins that help in removing the amyloid plaques from the brain. Dr. Das hypothesizes that inflammation helps clear plaque early in the development of Alzheimer's disease, but that at some point, continued production of the amyloid clumps in the brain overwhelms the ability of microglial cells to do their job. At that point, inflammation, chronically activated by presence of the amyloid plaque, can produce its own unhealthy effects on brain function.

[lynx]

curcumin and resveratrol modulate HDAC2, not sure if anyone else knows HDAC2 inhibitors offhand

Butyrate, a SCFA, which is produced by fermentation of fiber in the gut. Psyllium produces a lot of butyrate.

[Sillewater]

Right now curcumin comes to mind for beta-amyloid, niacinamide for tau protein tangles, and high-dose methylcobalamin to protect myelin and prevent brain atrophy. That's a good start -- if I knew anyone with alzheimer's I would have them serious doses of all three.

How much of each would you recommend?

[Mind]

Longevity Genes May Protect against Alzheimer's.

Considering these other discussions linking diabetes & Alzheimer's and homocysteine & Alzheimer's, and the apt definition of Alzheimer's as an age-related disease, this result should come as no surprise, at least on a subjective level to those who follow anti-aging research.

A genetic variation previously linked to longevity may also protect against the development of Alzheimer's disease and other types of dementia, according to a new study. The variant affects cholesterol metabolism, boosting levels of high density lipoprotein (HDL), also known as "good" cholesterol, but it's not yet clear how it could promote healthy aging in the brain. The new findings are likely to heighten interest in finding ways to chemically enhance good cholesterol--experimental drugs that mimic the molecular effects of the genetic variant are already in clinical tests for heart disease.

In a previous study of Ashkenazi Jews, researchers at Albert Einstein College of Medicine, in New York, found that a specific variation in a gene that codes for a protein called cholesteryl ester transfer protein (CETP) is more common in very long-lived people. Those older people who carried it also tended to have better cognitive function. (Ashkenazi Jews are often studied in genetic research because they originate from a relatively small founder population and possess less genetic complexity than other groups, making it easier to identify meaningful genetic targets.)

[mentatpsi]

I found this study rather interesting:

Both the Alzheimer's-prone mice and normal mice were then exposed to cell phone-level microwave radiation for two one-hour periods daily for seven to nine months.

The study found that if cell phone exposure began before the genetically engineered mice started showing signs of Alzheimer's, they were less likely to develop symptoms later on in life.

These mice performed as well on memory and thinking-skills tests as normal mice without Alzheimer's. For instance, the mice were given a cognitive interference task that tested their ability to remember something after an interruption. The team also put the mice through a three-armed Y maze, which measures basic memory function.... See More

Furthermore, the genetically engineered mice that were were exposed to the cell phone radiation after they had already begun to show cognitive deficits generally saw their memory impairment disappear after several months of the radiation exposure.

[mentatpsi]

Longevity Genes May Protect against Alzheimer's.

Considering these other discussions linking diabetes & Alzheimer's and homocysteine & Alzheimer's, and the apt definition of Alzheimer's as an age-related disease, this result should come as no surprise, at least on a subjective level to those who follow anti-aging research.

A genetic variation previously linked to longevity may also protect against the development of Alzheimer's disease and other types of dementia, according to a new study. The variant affects cholesterol metabolism, boosting levels of high density lipoprotein (HDL), also known as "good" cholesterol, but it's not yet clear how it could promote healthy aging in the brain. The new findings are likely to heighten interest in finding ways to chemically enhance good cholesterol--experimental drugs that mimic the molecular effects of the genetic variant are already in clinical tests for heart disease.

In a previous study of Ashkenazi Jews, researchers at Albert Einstein College of Medicine, in New York, found that a specific variation in a gene that codes for a protein called cholesteryl ester transfer protein (CETP) is more common in very long-lived people. Those older people who carried it also tended to have better cognitive function. (Ashkenazi Jews are often studied in genetic research because they originate from a relatively small founder population and possess less genetic complexity than other groups, making it easier to identify meaningful genetic targets.)

I'm not sure why no one commented prior, but great find.

[Mind]

Natural flavonoid mimics action of BDNF and protects brain cells (in animal models). Protection is great, but what we really want/need is rejuvenation.

"BDNF has been studied extensively for its ability to protect neurons vulnerable to degeneration in several diseases, such as ALS, Parkinson's and Alzheimer's disease," Ye says. "The trouble with BDNF is one of delivery. It's a protein, so it can't cross the blood-brain barrier and degrades quickly."

Working with Ye, postdoctoral fellow Sung-Wuk Jang sifted through a library of chemicals to find those that could stimulate one of the proteins on the surfaces of neurons that BDNF binds to. They could show that 7,8-dihydroxyflavone sends survival signals to brain cells by pulling together two TrkB receiver-dish molecules, just like BDNF does.

Moreover, it is active in the brain when injected into the body cavity, meaning that it can cross the blood-brain barrier. Ye says many experimental "neuroprotectant" drugs have been unsuccessful in clinical trials for diseases such as stroke and Parkinson's over the last decade.

"What's different is this is a new pathway, offering us new opportunities," he says. "This is the first molecule we've found that specifically triggers TrkB."

[Invariant]

Natural flavonoid mimics action of BDNF and protects brain cells (in animal models). Protection is great, but what we really want/need is rejuvenation.

"BDNF has been studied extensively for its ability to protect neurons vulnerable to degeneration in several diseases, such as ALS, Parkinson's and Alzheimer's disease," Ye says. "The trouble with BDNF is one of delivery. It's a protein, so it can't cross the blood-brain barrier and degrades quickly."

Working with Ye, postdoctoral fellow Sung-Wuk Jang sifted through a library of chemicals to find those that could stimulate one of the proteins on the surfaces of neurons that BDNF binds to. They could show that 7,8-dihydroxyflavone sends survival signals to brain cells by pulling together two TrkB receiver-dish molecules, just like BDNF does.

Moreover, it is active in the brain when injected into the body cavity, meaning that it can cross the blood-brain barrier. Ye says many experimental "neuroprotectant" drugs have been unsuccessful in clinical trials for diseases such as stroke and Parkinson's over the last decade.

"What's different is this is a new pathway, offering us new opportunities," he says. "This is the first molecule we've found that specifically triggers TrkB."

Curcumin also activates TrkB.

[tham]

Alpha GPC outperforms CDP choline in vascular dementia.

http://www.ncbi.nlm....st_uids=1916007

http://www.ncbi.nlm....st_uids=8030842



My father now has this condition in a nursing home. I've been
having a hard time trying to get across to my elder brother and
sister, who have never heard of life extension, that supplements
can help him when drugs can't even slow down the disease.

They think that life extension is "nonsense" (i.e. if highly-trained
specialists can't do much for aging, do you think your vitamin pills
can perform miracles ?).

Getting them to believe me, then for them to pass it on to the home
caregiver to give it to him, is an uphill battle.

The prognosis of vascular dementia is worse than Alzheimer's.

http://en.wikipedia....ity.2FMorbidity


They've just taken him to see some "geriatrician" in one of the private
hospitals here, who put him on a course of a transdermal patch drug,
probably one of the anticholinesterases. Cost M$600 for a month's supply,
plus M$200 consultation and M$100 for some blood test, and the total
bill came up to $900.


Alpha GPC against ALCAR.

http://www.ncbi.nlm....st_uids=8477148

[tham]

Vascular dementia.

http://www.ncbi.nlm....59/?tool=pubmed



Vitamin B12 and Alzheimer's.

http://www.ncbi.nlm....t_uids=20110595

ApoE4, C1 and Alzheimer's.

http://www.ncbi.nlm....t_uids=20145290

http://www.ncbi.nlm....t_uids=20102379



" Only a small proportion of patients with Alzheimer's disease
seem to benefit from the cholinesterase inhibitors tested "

http://www.tidsskrif...;art_id=1648831

[tham]

Galantamine in vascular dementia.

" Activities of daily living and behavioural symptoms were
also significantly improved. "

" Galantamine showed a therapeutic effect on all key areas of cognitive
and non-cognitive abilities in this group of dementia patients. "

http://www.ncbi.nlm....pubmed/11145488


Cholinesterase Inhibitors in BPSD (Behavioural and Psychological
Symptoms of Dementia).

http://www.ncbi.nlm....les/PMC2682404/



"Ultimate Alzheimer's Cocktail"


http://alzheimers.in...61/m/1891020913

[tham]

Several herbs or herbal formulas have been studied for dementia.
Two of them are Chinese formulas, which have also been used
by the Japanese.

Yi Gan San ( 义干山 ), based on bupleurum, called Yokukansan by
the Japanese.

Ba Wei Di Huang Wan ( 八味地黃丸 ), based around rehmannia.
Called Hachimi-jio-gan by the Japanese.

Lemon Balm (Melissa)

Sage (Salvia)



Yi Gan San helps BPSD, but not the cognitive decline.


http://www.acuatlant...es-p-45592.html

http://www.kalyx.com...5920.0/file.htm



http://www.naturalhe.....itions 2.html

http://ecam.oxfordjo...nt/full/3/4/441

http://www.webscienc...cfm?ID=20082073

http://article.psych...=52721817748969



Ba Wei Di Huang Wan helps both BPSD and cognitive decline.
It is normally taken for kidney support and is actually a very cheap
and common formula, with many manufacturers. Can be found in
any Chinese herbal shop in Malaysia.


http://www.hsusa.net...?products_id=41

http://www3.intersci...l...=1&SRETRY=0

http://www.ncbi.nlm....t_uids=15341554




Lemon Balm.

http://ecam.oxfordjo...;resid=74/7/863


Sage.

http://cel.isiknowle...mersID=Highwire

[tham]

On the earlier Japanese study of Ba Wei Di Huang Wan.

http://www.activeher...s20041026.shtml

[tham]

Chinese herbs in dementia.

http://www.itmonline.../alzheimers.htm

http://ecam.oxfordjo...ent/full/nep026


More on the Ba Wei Di Huang Wan study.

http://www3.intersci...l...=1&SRETRY=0



Donepezil in vascular dementia.

http://content.karge....1159/000088494

[tunt01]

dimebon failed

http://abcnews.go.co...tory?id=9998774


this was of a disappointing note, because it is thought to act upon mitochondria.

[tham]

Dang Gui Shao Yao San ( 当 归 芍 药 散 )

Also called Tong Kuei - Shao Yao San, or Angelica - Peony Formula.

Tokisha kuyaku-san by the Japanese.

This classic Chinese formula is normally used to treat women's problems,
but because angelica , peony and the other herbs in it are blood, kidney and
spleen supportive, has also been used for other conditions like anemia,
poor circulation, lumbago and general asthenia.

http://alternativehe...hao_yao_san.htm

http://www.cgcmall.c.../hr00dangsy.htm

http://www.acuatlant...ts-p-18984.html

http://eagleherbs.co...hao-yao-san-970



The earlier study shows benefit in post-stroke dementia.

http://ecam.oxfordjo...ent/full/nep026


Antioxidant and antiplatelet aggregation action as well.

http://www.ncbi.nlm....pubmed/16265987

[tham]

From the earlier link :

" According to traditional Chinese medicine, the depletion of
kidney - which is the dominant cause of symptoms associated
with aging - can be largely overcome by regular ingestion of
either Rehmannia Six Formula (Liu Wei Di Huang Wan) or
Rehmannia Eight Formula (Ba Wei Di Huang Wan) "


http://www.itmonline.../alzheimers.htm


During the mid-90s, I took a couple of bottles of Liu Wei
Di Huang Wan (Rehmannia Six formula, the baseline version
of Rehmannia Eight formula, Ba Wei Di Huang Wan) on
the recommendation of one lady, for kidney support.

I think I had better start taking it again, or better still,
Ba Wei Di Huang Wan.


Ba Wei Di Huang Wan is basically Liu Wei Di Huang Wan
with two extra herbs added. While the "Six" formula is more
for "Yin" support, the "Eight" formula is more for "Yang"
support.


http://en.wikipedia....ei_Di_Huang_Wan

http://www.activeherb.com/liuwei/

http://articles.dire...an-a853224.html

Edited by tham, 04 March 2010 - 07:10 PM.

[kismet]

Tham, I will seriously never understand how you cope with the cognitive dissonance. I.e. how you can manage to persue science-based treatments and things like faith-healthin, homeopathy, TCM based on yin and yang and folklore, etc. 

[mentatpsi]

Tham, I will seriously never understand how you cope with the cognitive dissonance. I.e. how you can manage to persue science-based treatments and things like faith-healthin, homeopathy, TCM based on yin and yang and folklore, etc. 

It is because of this open-mindedness that science is pursuing many of the botanicals, mushrooms and various other formulations purported by ancient medical systems. I am not sure how much research you do in this area, but if you have you must have noticed some validity there? Maybe not in the concepts of yin & yang and their extension into medicine, but rather in the herbs of lore and their mechanisms.

You must admit, without a market of this nature, many herbs would never be examined in a more empirical light.

[AgeVivo]

the depletion of kidney - which is the dominant cause of symptoms associated with aging

what does "depletion of kidney" mean?

Other subject:

What about Rember? I read that TauRX is still trying to get funding for a Phase III clinical trial. Do you know if it should start soon?
http://www.alzheimer...alzheimers.html

Edited by AgeVivo, 04 March 2010 - 09:11 PM.

[tham]

the depletion of kidney - which is the dominant cause of symptoms associated with aging

what does "depletion of kidney" mean?

The degeneration of kidney function with age.

That could be extrapolated to glycation, oxidation, AGES and the
consequential crosslinking in the kidney glomerules, which we all
eventually develop with age.

Since rehmannia and the other herbs in both the above formulas have
antidiabetic effects, it may explain such antiaging activity. Diabetes,
is after all, a model of accelerated aging.


http://www.ncbi.nlm....t_uids=15673189

http://www.ncbi.nlm....st_uids=2854548

http://www.jstage.js...8_1662/_article

http://www.ncbi.nlm....t_uids=15525452


http://www.ncbi.nlm....t_uids=17590296


Glycation is also involved in dementia.

" ..... glycation contributes to the formation of beta-amyloid, the
protein that clumps together in the brains of Alzheimer’s patients. "

http://websites.afar..._the_cross_glyc



" Researchers speculate that cross-linking of proteins in the
walls of arteries or the filtering systems of the kidney account
for at least some of the atherosclerosis (once called hardening
of the arteries) and age-related decline in kidney function
observed in older adults. Another study conducted at the
Bjorksten Institute in Wisconsin treated brain tissue from
young animals with known cross-link-inducing compounds.
That brain tissue soon looked quite similar to older brain tissue
with its naturally cross-linked brain proteins, adding evidence
in support of this theory of aging. "

http://www.healthand...er2_2.htm#cross

[tham]

In addition, traditional Chinese medicine centers around
supporting the kidneys.

In essence, we are "as healthy and old as our kidneys" .

When I visited a Chinese acupuncturist some years ago for
treatment of tinnitus, the first meridian she hit was that of
the kidneys.


http://www.shen-nong...ionkidneys.html

http://en.wikipedia....inese_medicine)

http://www.tcmstuden...ion Kidney.html

http://tcm.health-in...ion/kidneys.htm



More on rehmannia.

http://www.itmonline...rts/rehmann.htm


" Rehmannia is said to be the "Kidney’s own food." It is thus
believed to be a Kidney tonic and longevity herb and is found
in many common "anti-aging" formulations for longevity,
and rejuvenation. "

http://www.yahwehsal...iaprepared.html



" As a person gets old, as part of the natural aging process,
the energy reserves of the kidney are depleted. The energy
can be restored by taking remedies that tonifies the kidneys.
This is done primarily with herbal remedies. "

http://www.holistico...eep_ins_TCM.htm

Edited by tham, 05 March 2010 - 07:51 PM.

[tham]

The basic Rehmannia Six (Liu Wei Di Huang Wan) formula :

Rehmannia root 32%
Cornelian cherry 16%
Chinese yam 16%
Peony root bark 12%
Poria cocos 12%
Water plantain 12%


The basic Rehmannia Eight (Ba Wei Di Huang Wan) formula :

Rehmannia root 30%
Cornelian cherry 15%
Chinese yam 15%
Peony root bark 11%
Poria cocos 11%
Water plantain 11%

Plus :
Cinnamon bark 4%
Aconite root 4%


Many manufacturers have their own variants by
adding other herbs, such as Planetary Herbals's
"Rehmannia Vitalizer" :


http://www.vitasprin...-planetary.html


In Chinese :

"Liu" = Six
"Ba" = Eight

"Wei = Types
"Di Huang" = "Yellow Earth", the Chinese name for Rehmannia
"Wan" = Pills


Thus :

Liu Wei Di Huang Wan = Six Types Rehmannia Pills

Ba Wei Di Huang Wan = Eight Types Rehmannia Pills

[tham]

Herbs and dementia.

http://aja.sagepub.c...nt/21/2/113.pdf


I had recently emailed my brother presenting evidence to
on galantamine's effectiveness in vascular dementia,
along with studies on donepezil as a more cost-effective
option.

His reply, effectively tying my hands :

"Drugs have adverse effects. Galantamine takes 6 months
to work and is too expensive ..... "


He still doesn't realize that vascular dementia has a far
graver prognosis than Alzheimer's, even after I showed
him the Wikipedia page on it, and my father is going to
deteriorate fast IRREVERSIBLY without intervention.

" In contrast, the cognitive function deteriorated among those
in the placebo group. Patients with AD + CVD who were
switched from placebo to galantamine for the open-label
phase of the trial did show improvement in cognitive
function; however, they never attained the same cognitive
level as patients who had been treated with galantamine for
the entire 12 months. "


http://www.ncbi.nlm....t_uids=14560062


This replaces the earlier link on galantamine on vascular dementia,
which had erroneously been linked to one on rivastigmine.

http://www.ncbi.nlm....pubmed/11965273


Other studies on galantamine.

http://www.cnsforum....73/default.aspx

http://www.ncbi.nlm....pubmed/17664404



Alpha-GPC.

" The cholinergic precursor choline alfoscerate may be emerging
as a potential useful drug in the treatment of dementia, with few
adverse effects. "

http://www.ncbi.nlm....t_uids=14519085

[Sillewater]

Recent studies about Alzheimer's that have been popping up on my reader have been related to the connection between cholesterol and Abeta proteins/tangles. If you do a quick pubmed search many many many studies about how statins could decrease Alzheimer's or the connection between APOE allele E4/high cholesterol and the increased risk of AD, and in general dysregulation of cholesterol metabolism in the brain.

Most discussions and conclusions point towards high cholesterol as a culprit. However the first thing I tried to find was the connection between high serum cholesterol and cholesterol levels in the brain but couldn't find anything. But what I did find was some articles/reviews pointing out possible disconnects in this connection:

Biochem Soc Symp. 2005;(72):129-38.
The conflicting role of brain cholesterol in Alzheimer's disease: lessons from the brain plasminogen system.

Curr Alzheimer Res. 2009 Feb;6(1):15-29.
Cholesterol in Alzheimer's disease: unresolved questions.

[url="http://www.ncbi.nlm....7055"]Neurobiol Aging. 2009 Mar 16. [Epub ahead of print]
Membrane cholesterol enrichment prevents Abeta-induced oxidative stress in Alzheimer's fibroblasts.[/url]

Epidemiological evidence regarding cholesterol and AD:

Arch Neurol. 2007 Jan;64(1):103-7.
Twenty-six-year change in total cholesterol levels and incident dementia: the Honolulu-Asia Aging Study.

Some interesting reads that I haven't had time to go through:
Mol Cell Biochem. 2009 Jun;326(1-2):121-9. Epub 2008 Dec 31.
Why lipids are important for Alzheimer disease?

Brain Res Bull. 2010 Mar 3. [Epub ahead of print]
Lipid rafts: Keys to neurodegeneration.

Curr Alzheimer Res. 2009 Dec 1. [Epub ahead of print]
Cholesterol, Lipids, Amyloid Beta, and Alzheimer's.

Cholesterol Novel Target for Alzheimers (good overview from my skim)

AGEs and AD:
Neurobiology of Aging
Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease


Possible treatments:
Trends in Biochemical Sciences Volume 34, Issue 1, January 2009, Pages 6-8
No more brain tangles with ΔNp73

J Neurochem. 2007 Sep;102(6):1727-37. Epub 2007 Jun 15.
Oxysterols, cholesterol homeostasis, and Alzheimer disease.

Edited by Sillewater, 23 March 2010 - 10:46 PM.

[nito]

I don't know what it is but everytime i think of buying drugs to relieve dementia or alzeimers i get this thought that what if it brings about those conditions if you take these drugs since you don't suffer from it clinically lol.