Drug Found That Could Reduce Risk Of Alzheimer's

[Adsos Letter]

Source: ScienceDaily (Feb. 7, 2009)

A drug used to improve blood flow to the brain also could help improve learning and memory and reduce the risk of Alzheimer's disease, according to a new study released today by investigators at the Translational Genomics Research Institute (TGen) and Arizona State University.

Fasudil has been used for more than 10 years to help protect the brain in stroke patients by dilating blood vessels when blood flow is curtailed.

Now, a team of Arizona psychologists, geneticists and neuroscientists report in today's edition of the journal Behavioral Neuroscience that hydroxyfasudil, the active form of the parent drug Fasudil, improved spatial learning and working memory in middle-aged rats when negotiating a complicated maze.

The findings suggest that hydroxyfasudil may influence similar cognitive processes in humans involving the hippocampus, a part of the brain that has been shown to deteriorate in patients with age-related disorders.

http://www.sciencedaily.com/releases/2009/02/090202102932.htm

[crimsonblue]

1. there's another drug that has been associated with slowing/preventing many brain diseases

Marijuana.

[robinlynne]

2. not alzheimers. not at all. alzheimers is not a joke, and people with

serious brain problems (hippocampus) can't even go near alcohol or weed. Nothing aqgianst weed, but it does NOTHING to improve brain function. great for other things.

[bettyellen]

3. the latest research says it may help... look it up!

[robinlynne]

7. I'm on top of the altest research, constantly, have a mother with alzheimers,and stepfather

neurologist, so.....you look it up!

[tsuki]

15. I have a mother with alzheirmers, and I looked it up.

http://media.www.thelantern.com/media/storage/paper333/news/2009/01/27/Campus/Marijuana.Could.Prevent.Alzheimers-3598061.shtml

[bettyellen]

21. i have a mom with alzheimers and five people sent me that link....;-)

[tsuki]

25. I take Mom to UAB on the 18th. I'll ask them what they've heard.

Pretty progressive at UAB.

[bettyellen]

29. FYI: the research looks like it can prevent - not reverse AD.

[tsuki]

30. I have been told nothing can reverse it. Exelon and Namedia can

slow it, but after 35 years that's all they have.

BUT, BigPharma has conquered Restless Leg Syndrome.

[bettyellen]

22. i don't need to look it up- I'm aware of the studies, five people sent me the link

you're the one who seems to have missed it.
what do you think, you;re the only one "on top of " the research? hardly. my mom;s doc was the former president of the associaton of geriatric psychiatrists. possibly best treatment doc on the east coast.
put that n your pipe and smoke it.

[Ichingcarpenter]

6. not a joke- Read up on it rather than attack it

A puff a day might keep Alzheimer's away, according to marijuana research by professor Gary Wenk and associate professor Yannic Marchalant of the Ohio State Department of Psychology.

Wenk's studies show that a low dosage in the morning of a certain cannabinoid, a component in marijuana, reversed memory loss in older rats' brains. In his study, an experimental group of old rats received a dosage, and a control group of rats did not. The old rats that received the drugs performed better on memory tests, and the drug slowed and prevented brain cell death. However, marijuana had the reverse effect on young rats' brains, actually impairing mental ability.

Alzheimer's is a disease unique to humans and the memory loss in the rats was a natural decline, but rat brains are similar enough to human brains to serve as partial models for humans, Wenk said.
http://media.www.thelantern.com/media/storage/paper333/news/2009/01/27/Campus/Marijuana.Could.Prevent.Alzheimers-3598061.shtml

Marijuana may block Alzheimer's

The compound may protect the brain
The active ingredient in marijuana may stall decline from Alzheimer's disease, research suggests.
Scientists showed a synthetic version of the compound may reduce inflammation associated with Alzheimer's and thus help to prevent mental decline.

They hope the cannabinoid may be used to developed new drug therapies.

The research, by Madrid's Complutense University and the Cajal Institute, is published in the Journal of Neuroscience.

http://news.bbc.co.uk/2/hi/health/4286435.stm

Attacking Alzheimer's with Red Wine and Marijuana


Two new studies suggest that substances usually associated with dulling the mind -- marijuana and red wine -- may help ward off Alzheimer's disease and other forms of age-related memory loss. Their addition comes as another study dethrones folk remedy ginkgo biloba as proof against the disease.

At a November meeting of the Society of Neuroscience in Washington, D.C., researchers from Ohio State University reported that THC, the main psychoactive substance in the cannabis plant, may reduce inflammation in the brain and even stimulate the formation of new brain cells.

Meanwhile, in the Nov. 21 issue of the Journal of Biological Chemistry, neurologist David Teplow of the University of California, Los Angeles reported that polyphenols -- naturally occurring components of red wine -- block the formation of proteins that build the toxic plaques thought to destroy brain cells. In addition, these substances can reduce the toxicity of existing plaques, thus reducing cognitive deterioration.

Together, the studies suggest scientists are gaining a clearer understanding of the mechanics of memory deterioration and discovering some promising approaches to prevention.

Previous research has suggested that polyphenols -- which are found in high concentrations in tea, nuts and berries, as well as cabernets and merlots -- may inhibit or prevent the buildup of toxic fibers in the brain. These fibers, which are primarily composed of two specific proteins, form the plaques that have long been associated with Alzheimer's disease.

UCLA's Teplow and his colleagues monitored how these proteins folded up and stuck to each other to produce aggregates that killed nerve cells in mice. They then treated the proteins with a polyphenol compound extracted from grape seeds. They discovered the polyphenols blocked the formation of the toxic aggregates.

http://www.alternet.org/drugreporter/110806/attacking_alzheimer's_with_red_wine_and_marijuana/

[TZ]

13. This science is not cut and dry

See these studies//
http://www.sciencedaily.com/releases/2008/02/080213160851.htm
http://www.sciencedaily.com/releases/2008/10/081014111156.htm
http://www.sciencedaily.com/releases/2008/07/080707161411.htm
There is NO consensus on marijuana being helpful in brain diseases. None.

[eShirl]

16. "There is NO consensus on marijuana being helpful in brain diseases." ...yet.

[bettyellen]

23. of course not, the studies saying it may help are very new... there couln;t possily be consensus

but feel free to shit on it.
looks like a lot of people here assume they are the only ones with loved ones with az. would that it were true.

[Ghost in the Machine]

27. Ahem.... yes, marijuana *can* help people with Alzheimers

Alzheimer's


http://www.ncbi.nlm.nih.gov/pubmed/17140265?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
A molecular link between the active component of marijuana and Alzheimer's disease pathology.Eubanks LM, Rogers CJ, Beuscher AE 4th, Koob GF, Olson AJ, Dickerson TJ, Janda KD.
Department of Chemistry and Immunology, The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California 92037, USA.

Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Delta9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid beta-peptide (Abeta) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.
---

http://www.ncbi.nlm.nih.gov/pubmed/14657172?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer's disease brains.Benito C, Núñez E, Tolón RM, Carrier EJ, Rábano A, Hillard CJ, Romero J.
Laboratorio de Apoyo a la Investigación, Fundación Hospital Alcorcón, 28922 Alcorcón, Madrid, Spain.

The endocannabinoid system is still poorly understood. Recently, the basic elements that constitute it, i.e., membrane receptors, endogenous ligands, and mechanisms for termination of the signaling process, have been partially characterized. There is a considerable lack of information, however, concerning the distribution, concentration, and function of those components in the human body, particularly during pathological events. We have studied the status of some of the components of the endocannabinoid system, fatty acid amide hydrolase and cannabinoid CB1 and CB2 receptors, in postmortem brains from patients with Alzheimer's disease. Using specific polyclonal antibodies, we have performed immunohistochemical analysis in hippocampus and entorhinal cortex sections from brains of Alzheimer's disease patients. Our results show that both fatty acid amide hydrolase and cannabinoid CB2 receptors are abundantly and selectively expressed in neuritic plaque-associated astrocytes and microglia, respectively, whereas the expression of CB1 receptors remains unchanged. In addition, the hydrolase activity seems to be elevated in the plaques and surrounding areas. Thus, some elements of the endocannabinoid system may be postulated as possible modulators of the inflammatory response associated with this neurodegenerative process and as possible targets for new therapeutic approaches.
---


http://www.ncbi.nlm.nih.gov/pubmed/15728830?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation.Ramírez BG, Blázquez C, Gómez del Pulgar T, Guzmán M, de Ceballos ML.
Neurodegeneration Group, Cajal Institute, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain.

Alzheimer's disease (AD) is characterized by enhanced beta-amyloid peptide (betaA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. This background prompted us to study the localization, expression, and function of cannabinoid receptors in AD and the possible protective role of cannabinoids after betaA treatment, both in vivo and in vitro. Here, we show that senile plaques in AD patients express cannabinoid receptors CB1 and CB2, together with markers of microglial activation, and that CB1-positive neurons, present in high numbers in control cases, are greatly reduced in areas of microglial activation. In pharmacological experiments, we found that G-protein coupling and CB1 receptor protein expression are markedly decreased in AD brains. Additionally, in AD brains, protein nitration is increased, and, more specifically, CB1 and CB2 proteins show enhanced nitration. Intracerebroventricular administration of the synthetic cannabinoid WIN55,212-2 to rats prevent betaA-induced microglial activation, cognitive impairment, and loss of neuronal markers. Cannabinoids (HU-210, WIN55,212-2, and JWH-133) block betaA-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor-alpha release; these effects are independent of the antioxidant action of cannabinoid compounds and are also exerted by a CB2-selective agonist. Moreover, cannabinoids abrogate microglia-mediated neurotoxicity after betaA addition to rat cortical cocultures. Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.

---
http://www.ncbi.nlm.nih.gov/pubmed/17828287?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Alzheimer's disease; taking the edge off with cannabinoids?Campbell VA, Gowran A.
Department of Physiology and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland. [e-mail]

Alzheimer's disease is an age-related neurodegenerative condition associated with cognitive decline. The pathological hallmarks of the disease are the deposition of beta-amyloid protein and hyperphosphorylation of tau, which evoke neuronal cell death and impair inter-neuronal communication. The disease is also associated with neuroinflammation, excitotoxicity and oxidative stress. In recent years the proclivity of cannabinoids to exert a neuroprotective influence has received substantial interest as a means to mitigate the symptoms of neurodegenerative conditions. In brains obtained from Alzheimer's patients alterations in components of the cannabinoid system have been reported, suggesting that the cannabinoid system either contributes to, or is altered by, the pathophysiology of the disease. Certain cannabinoids can protect neurons from the deleterious effects of beta-amyloid and are capable of reducing tau phosphorylation. The propensity of cannabinoids to reduce beta-amyloid-evoked oxidative stress and neurodegeneration, whilst stimulating neurotrophin expression neurogenesis, are interesting properties that may be beneficial in the treatment of Alzheimer's disease. Delta 9-tetrahydrocannabinol can also inhibit acetylcholinesterase activity and limit amyloidogenesis which may improve cholinergic transmission and delay disease progression. Targeting cannabinoid receptors on microglia may reduce the neuroinflammation that is a feature of Alzheimer's disease, without causing psychoactive effects. Thus, cannabinoids offer a multi-faceted approach for the treatment of Alzheimer's disease by providing neuroprotection and reducing neuroinflammation, whilst simultaneously supporting the brain's intrinsic repair mechanisms by augmenting neurotrophin expression and enhancing neurogenesis. The evidence supporting a potential role for the cannabinoid system as a therapeutic target for the treatment of Alzheimer's disease will be reviewed herewith.

---
http://www.scientificfactsofpot.com/studies.htm#Alz

Research is a wonderful thing, isn't it?

:hi:

[krispos42]

4. And of course it doesn't cure it, but does require you to take it forever.

How... interestingly convenient.

[TZ]

10. nice

Say that to families of alzheimer's patients. I'm sure they'd be so thrilled that you feel the need to shit all over something that might help.

[krispos42]

19. In light of recent revelations about how Big Pharma shelved a promising line of ...

...diabetes-curing research for a dozen years and are only just now exploring it, I don't think wondering how the money was spent and how it wasn't spent is an unreasonable question.


Not that we'll ever know, of course.


But my dad's mom died with Alzheimers and it was horrible on everybody. My mom's mom is and dad's sister both have diabetes, and it's being especially hard on my grandmother due to her advanced age.

We'll take anything that works... and they know that.

I hope it works... but I also hope somebody makes something better.

[Deja Q]

26. Do you have a link for that national debt sig pic?

I'd love to print a larger version... :evilgrin:


And you're right. But as we all know, there is no profit in a cure.

Then again, with organic structures, and even inorganic ones, entropy is inevitable. In some cases, having to take it "forever" is an unfortunate reality.

[krispos42]

28. I already have for a guy at work...

:rofl:

Along with a certain Crooks&Liars article about Repubs voting for Bush's 1.4 trillion tax cut back in 2001 or 2002... :evilgrin:

[TahitiNut]

5. The "brain saver" ... useful for ischemic strokes and deadly for hemorrhagic strokes.

:shrug:

[Ichingcarpenter]

9. Four of the authors hold stock in Sygnis Pharma AG

The authors received financial support from the Evelyn F. McKnight Brain Research Foundation, the National Institute on Aging, the National Institute of Neurological Disorders and Stroke, and the state of Arizona. They maintain that they have no competing financial interests. Four of the authors hold stock in Sygnis Pharma AG, a German pharmaceutical company that owns the rights to develop this drug class as a potential memory enhancer.

[Oregone]

8. Pot helps too.

Just saying. If they could patent and bottle it, they wouldn't need this.

[TZ]

11. Thats not necessarily the case.

There is some research that shows that long term marijuana use is damaging to the memory. The science on the usefulness of marijuana on brain issues is NOT cut and dry.

[Oregone]

20. Im not referring to memory. Im referring to Alzheimers.

[TZ]

12. You know its a sad state of affairs

when instead of lauding something that could ease the suffering of a godawful disease, most of the resondents here are screaming BIG PHARMA conspiracy!
Fuck that shit. Anyone here know anybody with this disease? No? I'm betting you wouldn't be so goddamned callous if you did.

[MannyGoldstein]

14. Heavy Ibuprofin Use Associated With 50% Or So Less Alzheimer's

I believe that it's unknown as to whether the ibuprofin causes the drop in incidence, or is just correlated.

[dysfunctional press]

17. unfortunately, it may also promote heart failure...

http://www.emaxhealth.com/1020/80/28997/antiinflammatory-drugs-do-promote-heart-failure.html

Anti-Inflammatory Drugs do Promote Heart Failure

A new study shows that anti-inflammatory drugs do promote heart failure. The risk also increases with increased doses of the commonly sold drugs, such as naproxen and ibuprofen.

The study, published January 26, 2009 in the Archives of Internal Medicine, again shows the link between using drugs known as COX-2 inhibitors, and NSAID's (anti-inflammatory medicine). COX-2 inhibitors are drugs widely prescribed for pain, the most well known being Vioxx...

[bettyellen]

24. frequent use- not heavy! asprin is also thought to help.. whatever keeps your circulation

going and your BP lower helps.... unless of course it cause other prolems.

[Baikonour]

18. Let's so how quickly the pharmaceuticals push THIS one under the rug..