Alzheimer's

[budman]

Marijuana 'may stave off Alzheimer's'

From correspondents in Washington
October 05, 2006 06:17am
News.com.au
<blockquote>
GOOD news for ageing hippies - smoking pot may stave off Alzheimer's disease.
</blockquote>
New research shows that the active ingredient in marijuana may prevent the progression of the disease by preserving levels of an important neurotransmitter that allows the brain to function.

Researchers at the Scripps Research Institute in California found that marijuana's active ingredient, delta-9-tetrahydrocannabinol, or THC, can prevent the neurotransmitter acetylcholine from breaking down more effectively than commercially marketed drugs.

THC is also more effective at blocking clumps of protein that can inhibit memory and cognition in Alzheimer's patients, the researchers reported in the journal Molecular Pharmaceutics.

The researchers said their discovery could lead to more effective drug treatment for Alzheimer's, the leading cause of dementia among the elderly.

Those afflicted with Alzheimer's suffer from memory loss, impaired decision-making, and diminished language and movement skills.

The ultimate cause of the disease is unknown, though it is believed to be hereditary.

Marijuana is used to relieve glaucoma and can help reduce side effects from cancer and AIDS treatment.

Possessing marijuana for recreational use is illegal in many parts of the world, including the United States, though some states allow possession for medical purposes.

[palmspringsbum]

October 9, 2006
Science Daily

Marijuana's Active Ingredient May Slow Progression Of Alzheimer's Disease


Scientists are reporting discovery in laboratory experiments of a previously unknown molecular mechanism in which the active ingredient in marijuana may slow the progression of Alzheimer's disease (AD).

Scripps Research Institute's Kim D. Janda and colleagues used laboratory experiments to show that delta-9-tetrahydrocannabinol (THC) preserves brain levels of the key neurotransmitter acetylcholine.

Existing medications for AD, including donepezil and tacrine, also relieve AD symptoms by inhibiting the enzyme, acetylcholinesterase, which breaks down acetylcholine.

THC does so by inhibiting an alternative site on acetylchlolinesterase and at lower concentrations, Janda's group reports in an article in the current (Oct. 2) issue of the ACS bimonthly journal, Molecular Pharmaceutics. Their experiments show that THC also prevents formation of the amyloid plaques that are a hallmark of AD and its damage to the brain.

"Our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology," they state. They also note that THC may provide a "drug lead" -- a model for developing new and more effective medications with more targeted effects on AD.

The researchers explain that such compounds "may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reeducating amyloid beta aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease."

[palmspringsbum]

Pot helps in fighting Alzheimer's, study says

Ashton Shurson - The Daily Iowan
Posted: 10/10/06

While antidrug advertisements may plaster television screens and magazines, a new medical study may add another check to the list of marijuana's beneficial uses.

A recent study by the Scripps Research Institute in California found that the active ingredient in the illegal plant - tetrahydrocannabinol, or THC - may halt the progression of Alzheimer's disease. THC helps stop the formation of amyloid plaque, which primarily causes the disease, the report stated.

The institute found THC to be " 'a considerably superior inhibitor of [amyloid plaque]' to several currently approved drugs for treating the disease."

"While we are certainly not advocating the use of illegal drugs, these findings offer convincing evidence that THC possesses remarkable inhibitory qualities," especially when compared with other medicines available to patients, said Kim Janda, a chemistry professor at Scripps Research, on the institute's website.

Although many local doctors haven't researched this subject, some are interested in the topic, they said.

"I've never heard of anything like this before," said Daniel Tranel, a UI professor of neurology. "There is a lot of intrigue and promise."

The report, which was published in the journal Molecular Pharmaceutics, a publication of the American Chemical Society, said in addition to slowing down the progression of Alzheimer's, THC can also treat symptoms of the disease.

Tranel said Alzheimer's is not preventable and that current drugs are "mediocre at best at slowing symptoms in some patients."

"If this is replicated and extended, it could be very helpful," he said.

Roughly 4.5 million Americans have Alzheimer's; in 2050, experts project that the disease will afflict as many as 16 million people, according to the Alzheimer's Association.

The disease - a leading cause of dementia - slowly takes over a person's memory and ability to learn, reason, make judgments, communicate, and carry out daily activities, according to the association.

Currently, recreational marijuana use is illegal in all states, but medicinal marijuana is legal in 11 states (none of which are named Iowa). It can help ease pain and nausea in cancer patients, and Tranel said it can also stimulate appetite.

Locally, many students use marijuana for personal reasons, and many favor legalizing the drug. UI sophomore Adam Filarski, who created the Facebook group "I Heart Blunts," supports legalizing marijuana, although he is not very active in the fight.

"The government spends so much money promoting illegalization of it, and it could be" spending it on other things, he said. "It has proven no reason people shouldn't be allowed to do that. The government needs to let people make certain decisions."

E-mail DI reporter Ashton Shurson at:
ashton-shurson@uiowa.edu

[palmspringsbum]

CORRECTED: Marijuana may stave off Alzheimer's: study

Tue Oct 10, 2006 11:35 PM BST

<b><span class=postbold>Corrects the nature of THCs action in paragraphs 2 and 3</span></b>

By Andy Sullivan
Reuters UK

WASHINGTON (Reuters) - Good news for aging hippies: smoking pot may stave off Alzheimer's disease.

New research shows that the active ingredient in marijuana may prevent the formation of deposits in the brain associated with the degenerative disease.

Researchers at the Scripps Research Institute in California found that marijuana's active ingredient, delta-9-tetrahydrocannabinol, or THC, can prevent an enzyme called acetylcholinesterase from accelerating the formation of "Alzheimer plaques" in the brain more effectively than commercially marketed drugs.

The researchers said their discovery could lead to more effective drug treatment for Alzheimer's, the leading cause of dementia among the elderly.

Those afflicted with Alzheimer's suffer from memory loss, impaired decision-making, and diminished language and movement skills. The ultimate cause of the disease is unknown, though it is believed to be hereditary.

Marijuana is used to relieve glaucoma and can help reduce side effects from cancer and AIDS treatment.

Possessing marijuana for recreational use is illegal in many parts of the world, including the United States, though some states allow possession for medical purposes.

[palmspringsbum]

<span class=postbold>Study:</span> Marijuana's active ingredient may actually improve memory

James Heggen
Iowa State Daily

October 12, 2006

(AMES, Iowa) - It seems sacrificing your memory now could lead to saving it in the future.

A new study, published in the journal Molecular Pharmaceutics by researchers at the Scripps Research Institute in California has found that the active ingredient in marijuana may prevent the progression of Alzheimer's disease.

The link between marijuana and Alzheimer's disease lies in the active ingredient, said Dr. Robert Bender, geriatrician at the Johnny Orr Memory Center and Healthy Living Institute, who specializes in diseases of old age with an interest in memory disorder.

"What various studies around the world are starting to show is that the basic ingredient in marijuana, the cannabis, may actually increase the level of a neurotransmitter called acetylcholine, which we need to form new memories," Bender said. "It also may block the formation of something called amyloid plaques."

Amyloid plaques are very common in the brains affected by Alzheimer's disease and may be a key to why patients develop the disease, Bender said. Plaques result when the brain cannot breakdown amyloid normally. The resulting build-up of plaques impair brain function and nerve transmission.

He also said researchers have found that the cannabis may decrease inflammation in the brain of patients who have Alzheimer's disease.

"Inflammation is something that results from whatever is going on in the brain to lead to Alzheimer's disease and there is some feeling that if we can decrease the inflammation, the process may be slowed down, that is the process of deterioration that patients experience," he said.

In Bender's opinion, since this research doesn't get at the cause of Alzheimer's, it will probably lead to a treatment, rather than a cure.

"Even in the most optimistic view, it probably will not be a cure. It may be something that leads us to develop another way of slowing the progress down," he said.

If you're wondering how the active ingredient in marijuana promotes memory, but you still can't remember where you put your keys, Bender has some insight.

"It's probably because of, as far as I can tell, the sedating effect of the drug, the way that people take it. When you're sedated, you're not alert and when you're not alert, you don't remember things as well," Bender said.

For those of you on your way to go smoke some pot in the name of neurological health, Bender would suggest you put down the bong.

"We certainly would never recommend that people smoke marijuana to prevent Alzheimer's disease," Bender said.

Smoking marijuana will not be the solution for treatment of Alzheimer's disease in Bender's opinion. What he expects is that there will be much work to refine and isolate chemicals in order to get the positive effects without the intoxicating side effects.

"The cannabinoid that is in marijuana will probably have to be refined and people would have to find ways to make sure that the side effects don't outweigh the potential benefits," he said. "I feel confident that we will not be prescribing for people to smoke marijuana, but it may be that they can isolate chemicals, perhaps alter them a little bit that are in marijuana and eventually use them therapeutically."

This study will lead to more research in trying to harness the active ingredient in marijuana in a medication form rather than medical marijuana use, said Rep. James Kurtenbach, R-Nevada.

"What I would expect to happen is if the active ingredient that impacts marijuana can be isolated that can be used in a form such as a tablet or pill or chemical injection then the research would try to harness that active ingredient," he said.

Kurtenbach does not believe public support for the use of marijuana medically will not change either.

"Alzheimer's is an extremely terrible disease," he said. "Any medication that will less the impact or delay the impact of Alzheimer's will drive public support towards increased funding, however I don't believe that it would drive public support simply for licensing for medical marijuana."

Rep. Beth Wessel-Kroeschell, D-Ames, said there have been other medicinal uses of marijuana, and this may shift the way marijuana is used and viewed in society.

"I know people have seen the benefits of using marijuana for these purposes, have really struggled to get approval for that from the FDA," she said.

"It's always been a big struggle because of the negatives that surround marijuana, but this is a big study, a big step in an interesting direction."

From what Wessel-Kroeschell read, she believed more research needs to take place and stressed that this type of medicine should always be monitored by a doctor.

Wessel-Kroeschell said she felt the new findings could add fresh support to the pro-marijuana lobby.

"I think that in families that have been seriously affected by [Alzheimer's], certainly any hope that's out there brings them out of the woodworks looking for support," she said.

"It does have the potential to change the impression of the public."

And what if there isn't _one_ active ingredient?

And what is your basis for assuming there is one and only one -active- ingredient?

What if it's the profile of the 400 or so other chemicals in cannabis that cause it to be effective. What if the whole (as we've seen time and time again with cannabis) is greater than the sum of its parts?

[palmspringsbum]

Here is where the quest for a -single- active chemical, or magic bullet has gotten us...

Atypical Antipsychotics Get Poor Grade for Alzheimer's Psychoses

<small>By Neil Osterweil, MedPage Today Staff Writer
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
October 11, 2006
MedPage Today</small>


<table class=posttable align=right width=260><tr><td class=postcell><span class=postbold>MedPage Today Action Points</span>
<ul class=postlist>
<li>Explain to patients that agitation, aggression, delusions, hallucinations, and other forms of psychosis are common in patients with more advanced stages of Alzheimer's disease. </li>

<li>Explain that two of three second-generation antipsychotic drugs do not appear to control psychosis in patients with Alzheimer's disease, and are not approved by the FDA for this indication. </li>

<li>Point out that because of adverse side effects, none of the three drugs appeared to be clinically beneficial. </li>
</ul>
</td></tr></table>LOS ANGELES, Oct. 11 -- Two of three atypical antipsychotic drugs were no better than placebo at quieting aggression, psychosis, and agitation in patients with Alzheimer's disease, found a multicenter trial.

Overall, the adverse effects of all three outweighed the benefits, Lon S. Schneider, M.D., of the University of Southern California, and colleagues, reported in the Oct. 12 issue of the New England Journal of Medicine. In the study of more than 400 such Alzheimer's patients, a majority were taken off the drugs.

In addition, up to a quarter of the patients taking the drugs dropped out because of adverse effects, compared with only 5% of those given placebo.

The study suggests that the atypical antipsychotics Zyprexa (olanzapine), Risperdal (risperidone), and Seroquel (quetiapine) do not provide significant clinical benefits in patients with Alzheimer's, the investigators wrote.

"Antipsychotic medications have been used extensively for Alzheimer's patients without enough solid evidence of whether they are effective," said Thomas R. Insel, M.D., director of the National Institute of Mental Health, which funded the study.

"The study has vital public health implications because it provides physicians and patients with information to more accurately weigh the medications' benefits against their drawbacks, with the needs and unique reactions of their individual patients," Dr. Insel said.

Atypical antipsychotic agents have revolutionized the treatment of schizophrenia and other conditions with psychotic components, but these agents are not approved for use in older patients with dementia.

In fact, the drugs carry an FDA-mandated black-box warning stating that "elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs are at an increased risk of death compared to placebo," noted Jason Karlawish, M.D., of the Institute on Aging at the University of Pennsylvania, in an accompanying editorial.

To determine whether the drugs could play a role in controlling the symptoms of outpatient Alzheimer's patients, Dr. Schneider and co-investigators in the Clinical Antipsychotic Trials of Intervention Effectiveness -Alzheimer's Disease (CATIE-AD) study conducted a 42-site, double-blind, placebo-controlled trial.

The 421 participants had who exhibited delusions, hallucinations, aggression, or agitation that developed after the onset of dementia and was judged to be severe enough to disrupt their function and warrant treatment with antipsychotic agents.

The patients were randomly assigned to Zyprexa at a mean dose of 5.5 mg per day, Seroquel at a mean dose of 56.5 mg per day, Risperdal at a mean dose of 1.0 mg per day, or placebo. The drug doses were adjusted as needed, and patients were followed for up to 36 weeks.

The primary study outcomes were the time from the start of treatment to discontinuation for any reason, and the number of patients with at least a minimal improvement on the Clinical Global Impression of Change scale at 12 weeks.

The authors found that there were no significant differences among the groups with regard to discontinuation of treatment for any reason. The median time for patients to be taken off Zyprexa was 8.1 weeks, compared with 5.3 weeks Seroquel, 7.4 weeks for Risperdal, and 8.0 weeks for placebo (P=0.52).

When they looked at discontinuations due to lack of efficacy, they found that patients were kept on Risperdal and Zyprexa for significantly longer than either Seroquel or placebo. The median time for discontinuation due to lack of efficacy of Risperdal was 26.7 weeks, and for Zyprexa was 22.1 weeks, compared with 9.1 weeks for Seroquel, and 9.0 weeks for placebo (P=0.002).

When the investigators focused on discontinuation of treatment due to adverse events or intolerability, they found that 24% of patients who received Zyprexa, 16% who received Seroquel, 18% who received Risperdal were taken off their respective drugs, compared with 5% of patients who received placebo. The difference was significant in favor of placebo (P=0.009).

Overall, there were no significant differences among the groups with regard to improvement on the Clinical Global Impression of Change scale, with 32% of patients assigned to Zyprexa, 26% on Seroquel, 29% on Risperdal and 21% assigned to placebo having at least a minimal degree of improvement (P=0.22).

Zyprexa was significantly better than placebo (P=0.05) on initial assessment with the Cox model but not when compared with placebo by means of a Hochberg adjustment for multiple comparisons.

"Overall, the rates of discontinuation of treatment among the four study groups ranged from 77% to 85%, the authors wrote. "Although the differences among the groups may have been significant in a larger trial, our findings suggest that there is no large clinical benefit of treatment with atypical antipsychotic medications as compared with placebo."

They concluded, "Although the atypical antipsychotic drugs were more effective than placebo, adverse effects limited their overall effectiveness, and their use may be restricted to patients who have few or no side effects and for whom benefits can be discerned. Clinicians, patients, and family members must consider both risks and benefits in order to optimize a patient's care."

In his editorial, Dr. Karlawish hailed the CATIE-AD study as "an exemplar of the clinical trial's revolutionary role in shaping therapeutics. Recent remarks by FDA officials support wider use of these kinds of adaptive designs. This trial, funded by the National Institutes of Health, is also a model for how to spend our taxes on research, particularly now that taxes also pay for prescriptions."

Primary source: New England Journal of Medicine
Source reference:
Schneider LS et al. "Effectiveness of Atypical Antipsychotic Drugs in Patients with Alzheimer's Disease." N Engl J Med 2006;355:1525-38.

[palmspringsbum]

Latest Buzz: Marijuana May Slow Progression Of Alzheimer's Disease

New evidence in rats suggests that marijuana may contain compounds that slow the memory loss associated with Alzheimer's disease

Science Daily
October 18, 2006

Marijuana has strong anti-inflammatory effects, and many researchers believe that there is a compelling link between chronic inflammation and the progression of Alzheimer's, said Gary Wenk, a study co-author and a professor of psychology at Ohio State University.

“Inflammation in the brain is part of aging,” Wenk said. “It happens to almost all of us as we age. But in some cases, this inflammation gets out of hand and causes serious damage.”

Treatment with a synthetic compound similar to marijuana reduced inflammation in older rats in addition to making the animals “smarter,” said Wenk, who is also a professor of neuroscience and molecular virology, immunology and medical genetics.

“The compound substantially improved the memories of the older rats,” he said. “These animals were able to hold on to key details of a specific task. Untreated older rats, on the other hand, were not.”

The researchers presented their findings October 18 in Atlanta at the annual Society for Neuroscience meeting.

Evidence suggests that people who regularly smoked marijuana in the 1960s and 1970s rarely develop Alzheimer's disease, said Wenk, adding that researchers are eager to develop a drug with the anti-inflammatory properties of marijuana, but without the drug's psychoactive effects.

The colleagues treated young and old rats with WIN-55212-2 (WIN), a synthetic drug similar to marijuana. While the compound improved memory and helped to control inflammation, it is not a candidate for use in humans because it still contains substances that could trigger a high.

“We don't use marijuana in our experiments because we're trying to find a compound that isn't psychoactive,” Wenk said. “And using synthetic compounds may eventually help us to separate the beneficial effects from the psychoactive effects.”

The researchers inserted a small tube into the brain of each rat. The tubes were kept in place for three weeks to allow for periodic infusion of lipopolysaccharide (LPS) a material that stimulates an immune reaction. LPS triggers a reaction that mimics the inflammation found in Alzheimer's patients.

Some of the rats were also treated with WIN daily for those three weeks.

The animals were subjected to a memory test during the third week of treatment. They navigated a water maze that requires finding an escape platform hidden just below the surface of opaque water. The rats were given several opportunities over three days to acclimate to the water maze. On the fourth day, the researchers timed how quickly each rat found the platform.

“The maze task is sensitive to memory impairment and also to aging,” Wenk said. “Old rats tend to be pretty bad at navigating the maze. It's kind of like an elderly person trying to find his way around a house that he's not familiar with.

Once the testing was complete, the researchers began to examine the animals' brains for signs of inflammation – they looked for certain kinds of immune cells that are typically found in large quantities in the brains of former Alzheimer's patients.

They found that the marijuana-like compound decreased inflammation in the brains of young and old rats, and that the treated animals in both age groups could find the platform in the water faster than the non-treated animals.

But the most noticeable difference was between the treated and non-treated older rats.

“The compound significantly improved the older rats' memories,” Wenk said. “They found the platform faster, suggesting that they were less apt to forget key information for this task. It's a pretty good prediction of how a human would respond to this drug.”

Younger rats treated with the compound found the escape platform faster than non-treated younger rats did. However, the difference wasn't as remarkable as that of the older group, possibly due to the lack of age-related changes in the brains of the younger rats.

“Older rats have impaired spatial memory, due to the effect of aging on the brain,” Wenk said.

Wenk conducted this work with Ohio State colleagues Yannick Marchalant and Francesca Cerbai, both postdoctoral researchers in psychology, and Holly Brothers, a graduate student in psychology.

This ongoing work is supported by a grant from the National Institutes of Health.

[palmspringsbum]

Society For Neuroscience: Marijuana May Slow Memory Loss In Alzheimer's Patients

All Headline News

October 18, 2006 11:36 p.m. EST

Russell McSpadden - All Headline News News Writer

Atlanta, GA (AHN) - New medical research suggests that marijuana may slow the progression of Alzheimer's. The finding was presented at the annual meeting of the Society for Neuroscience in Atlanta on Wednesday.

Researchers from Ohio State University in Columbus found a compound present in marijuana that can help slow memory loss by reducing brain inflammation.

The experiment involved the use of rats placed in a maze. One psychology professor, Gary Wenk, began the experiment based on pre-existing evidence that marijuana users had lower rates of Alzheimer's than the population at large.

"We are using a component of marijuana that stimulates the same centers in the brain that marijuana does," Wenk said. The team developed a synthetic compound, based on composition found in marijuana, called WIN-55212-2 (WIN).

According to the study, the compound proved effective. The use of the compound on rats proved to be "a very effective anti-inflammatory, it reduces brain inflammation," Wenk said. The compound "reversed the memory impairment in the older rats," he said.

As of yet, the synthetic compound has not been approved for human subjects, and it still carries the ingredients which produce the "high" of the plant. Nevertheless, Wenk hopes that the compound can be used to treat patients soon. He does not, however, suggest that Alzheimer's suffers consume marijuana, stating that at unregulated doses, the drug would only increase such symptoms as dementia and memory loss.

[palmspringsbum]

<span class=postbold><i>“Anti-inflammatories in plants and antioxidants are a dime a dozen,” Wenk says. “They’re just everywhere.”

“The important thing, though, is that they not have too many side effects and that they actually get in the brain.

“So that’s what makes a … drug like a cannabinoid so useful,” he explains.

“It [this compound] does something that no other anti-inflammatory that I’ve tested in our model has ever done, and that’s that it reduces inflammation in an old brain,” Wenk says. “Old brains are different than young brains.”</i></span>

Marijuana-Like Compound May Slow Alzheimer's

Thursday , October 19, 2006

By Miranda Hitti

Fox News


<span class=postbold>A marijuana-like compound may cut brain inflammation and slow the progression of Alzheimer’s disease, scientists report.</span>

The compound is a synthetic cannabinoid, made in a lab to resemble marijuana.

Old rats given the compound performed better in a maze, according to research by Gary Wenk, PhD, professor of psychology and neuroscience at Ohio State University, and others.

What about people? “Now, I don’t know, because I’m just a rat guy, whether this is going to work that well in humans,” Wenk tells WebMD. “But it looks like it will, because of what we’ve seen with other drugs in other diseases.”

The marijuana-like drug “won’t cure the disease, but what it might do is stop the processes that are involved in making the disease worsen,” Wenk says. “I think that’s the most exciting aspect.”

“What may matter is that we can tell people that we might be able to step in, stop the inflammation, and they might die of old age before the inflammation has a chance to rebuild itself, which we believe takes many decades,” Wenk says.

“That’s the main hope, I think,” he says.

Who Gets Alzheimer’s? Genes Hold Key

<span class=postbold>Reducing Brain Inflammation</span>

Wenk’s team tested the synthetic cannabinoid to curb brain inflammation in rats.

“We know that brain inflammation at a low level plays a role in lots of diseases” including Alzheimer’s, Wenk explains.

“Now inflammation in all these conditions doesn’t cause the disorder,” he says. But, “it has consequences.”

“In fact, the inflammation appears long before plaques and tangles and memory impairment,” Wenk says, referring to the plaques and tangles seen in the brains of people who die with Alzheimer’s disease.

<span class=postbold>Rat Trials</span>

For their study, researchers looked at young and old male rats.

Some of the rats got the cannabinoid drug; others got a drug-free placebo. The rats received the drug or placebo through shots or a pump hooked up to their bodies.

Results showed less brain inflammation with the drug than with the placebo.

Plus, older rats taking the drug outperformed their placebo peers on a memory test involving a watery maze.

“Now, we didn’t make them as smart as young rats. Nothing does that yet,” Wenk says. “But we lessened the impairment by half.”

“We’ve tested the animals’ memory ability in a task that’s vulnerable to aging, and then given them a drug to see if it could reduce their inflammation,” Wenk says. “And we cut it down by 50 percent to 90 percent, depending on what part of the brain you look at.”

<span class=postbold>No 'High'</span>

“I’m not recommending that [people] go out and smoke marijuana,” Wenk says.

“We have to produce this anti-inflammatory effect at a dose that doesn’t make our rats high or impaired,” he says. “This is a psychoactive compound and it is regulated for that reason.”

“Now, I don’t know what it means to be high if you’re a rat, but I do know if you are high, you probably are memory-impaired; your attention is impaired,” Wenk says.

<span class=postbold>Why This Drug?</span>

“Anti-inflammatories in plants and antioxidants are a dime a dozen,” Wenk says. “They’re just everywhere.”

“The important thing, though, is that they not have too many side effects and that they actually get in the brain.

“So that’s what makes a … drug like a cannabinoid so useful,” he explains.

“It [this compound] does something that no other anti-inflammatory that I’ve tested in our model has ever done, and that’s that it reduces inflammation in an old brain,” Wenk says. “Old brains are different than young brains.”

<span class=postbold>Alzheimer’s Prevention?</span>

The drug hasn’t been tested against Alzheimer’s in people.

But if the research pans out, people might one day take such drugs to head off Alzheimer’s decades later, Wenk notes.

“The problem is, who would take it?” he says. “We don’t have reliable early tests [for Alzheimer’s] -- not yet.”

“So do we have to treat everyone? Well, that ends up being very expensive. We don’t have an answer to that question yet,” Wenk says.

Much more work lies ahead, but Wenk sounds hopeful.

“This is something that might actually happen in my lifetime, before I get to the point where I have to worry about it,” Wenk says. “So from that standpoint, I think it’s very positive.”


<hr class=postrule>
By Miranda Hitti, reviewed by Louise Chang, MD

<i>SOURCES: Society for Neuroscience’s annual meeting, Neuroscience 2006, Atlanta, Oct. 14-18, 2006. Gary Wenk, PhD, professor, departments of psychology and neuroscience &amp; molecular virology, immunology, and medical genetics, Ohio State University.</i>

[palmspringsbum]

Weekend Edition
October 20 / 22, 2006

<b><big><span class=postbold>Pot Shots</span></big></b>

Corporate Drugs Useless Against Alzheimer's

By FRED GARDNER
CounterPunch

Eli Lilly, Johnson &amp; Johnson, and AstraZeneca have been making $2 billion a year selling useless pills to Alzheimer's patients (including almost a million Medicare "beneficiaries"). This is the bottom line of a study published this week in the New England Journal of Medicine that evaluated the effectiveness of Seroquel, Risperdal and Zyprexa, drugs known as "atypical antipsychotics," which are routinely prescribed to Alzheimer's patients. A group led by Lon Schneider, MD, at the University of Southern California School of Medicine found that 80% of Alzheimer's patients they studied stopped taking the drugs before the trial ended due to ineffectiveness and side-effects.

The study was funded by the National Institute of Mental Health, whose director, Thomas R. Insel, commented "We need to come up with better medications." Indeed -more than 4.5 million Americans have been diagnosed with Alzheimer's. Its environmental causes remain unknown (the fake food must factor in) and it is occurring with increasing frequency.

The rage associated with Alzheimer's is one of the conditions for which Oregon doctors can authorize cannabis use. Perhaps Dr. Insel should fund a study of its efficacy there -it's just a matter of collecting the data.

Paul Armentano of NORML has summarized the recent scientific literature on cannabinoid therapy for Alzheimer's patients. It looks promising:<blockquote>Writing in the February 2005 issue of the Journal of Neuroscience, investigators at Madrid's Complutense University and the Cajal Institute in Spain reported that administration of the synthetic cannabinoid WIN 55,212-2 directly to the brain prevented cognitive impairment and decreased neurotoxicity in rats injected with amyloid-beta peptide (a protein believed to induce Alzheimer's). Other cannabinoids were also found to reduce the inflammation associated with Alzheimer's disease in human brain tissue in culture. "Our results indicate that ... cannabinoids succeed in preventing the neurodegenerative process occurring in the disease," investigators concluded.

Investigators at The Scripps Research Institute in California have reported that THC inhibits the enzyme responsible for the aggregation of amyloid plaque -the primary marker for Alzheimer's disease- in a manner "considerably superior" to approved drugs such as donepezil and tacrine.

"Our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology," researchers concluded. "THC and its analogues may provide an improved therapeutic [option] for Alzheimer's disease [by]... simultaneously treating both the symptoms and the progression of [the] disease." Previous preclinical studies have demonstrated that cannabinoids can prevent cell death by anti-oxidation. Some experts believe that cannabinoids' neuroprotective properties could also play a role in moderating Alzhemier's.

Clinical trials also indicate that cannabinoid therapy can reduce agitation and stimulate weight gain Alzheimer's patients. Investigators at Berlin 's Charite Universitatmedizin, Department of Psychiatry and Psychotherapy have reported that the daily administration of 2.5 mg of synthetic THC over a two-week period reduced nocturnal motor activity and agitation in Alzheimer's patients in an open-label pilot study.

Clinical data presented at the 2003 annual meeting of the International Psychogeriatric Association previously reported that the oral administration of up to 10 mg of synthetic THC reduced agitation and stimulated weight gain in late-stage Alzheimer's patients in an open-label clinical trial. Weight gain and a decrease in negative feelings among Alzheimer's patients administered cannabinoids had been reported by investigators in the International Journal of Geriatric Psychiatry in 1997.</blockquote>The U.S. now has a two-tier system of medical expertise; there are doctors who have educated themselves about the endocannabinoid system and the drugs that affect it, and doctors who have not. Unfortunately, the head of the National Institute of Mental Health is in the lower tier. A soon-to-be published survey of California doctors who have approved cannabis use by more than 100,000 patients asked, among other things, "What drugs has cannabis enabled your patients to discontinue or use less of?" All the respondents mentioned atypical antipsychotics. No wonder the pharmaceutical companies -and the corporations they interconnect with, i.e. petrochemicals, agribiz, banks- are committed to Prohibition.

Fred Gardner is the editor of O'Shaughnessy's Journal of the California Cannabis Research Medical Group. He can be reached at: fred@plebesite.com

[palmspringsbum]

Nov. 29, 2006

Company to start human trials on Alzheimer's drug

Medication has proven effective in clearing plaque in brains of animals

By ANNETTE WELLS
REVIEW-JOURNAL

A Las Vegas pharmaceutical company expects to begin human trials early next year of a drug it believes has the potential to delay or stop the progression of Alzheimer's.

The drug, known as caprospinol, has proven effective in clearing plaque, known as beta-amyloid, in the brains of animals, said Janet Greeson, chief executive officer of Samaritan Pharmaceuticals, which is located along Convention Center Drive.

Beta-amyloid is viewed by many scientists as the cause of degeneration and dementia in people with Alzheimer's, Greeson said.

"It's the same as when we were looking for heart medication that cleared plaque out of the heart,'' she said of caprospinol's potential.

"This is the real deal. It completely clears beta-amyloid in animals, and there is a good indication that it will do it in humans.''

Samaritan Pharmaceuticals, which has been in Nevada since 1994 and has a lab at Georgetown University, submitted an Investigational New Drug application to the FDA for caprospinol on Oct. 29, Greeson said.

Tom Lang, chief drug development officer for Samaritan Pharmaceuticals, said Tuesday that the U.S. Food and Drug Administration had 30 days to question the company about the drug, and the company has answered all of the agency's questions so far.

The 30-day period ends today, so barring any eleventh-hour questions, Samaritan Pharmaceuticals should be cleared to begin human trials as of Thursday, Lang said.

"We don't think there are going to be any major hold-ups,'' he said. "We have had answers to all of their questions.''

Dr. Charles Bernick, professor of medicine at the University of Nevada's School of Medicine, said first phase clinical trials of caprospinol could begin as early next year.

Bernick, who is involved in other Alzheimer's studies and in the development of the Lou Ruvo Brain Institute in Las Vegas, was approached by Samaritan Pharmaceuticals a few months ago about participating in the human trials.

"There are a lot of different strategies being looked at with respect to Alzheimer's treatment, and now the approach is looking for agents that will affect the disease's projectory,'' Bernick said.

"Most other drugs don't change the disease's progression, whereas this drug and other agents target the disease process itself. It has the potential to delay and slow the progression, which would be huge.''

Alzheimer's is a degenerative brain disease. It usually begins with a gradual forgetfulness about recent events or familiar tasks.

In later stages, the person has difficulty communicating, often struggling to find words, finish their thoughts or follow directions.

According to federal statistics an estimated 4.5 million Americans have Alzheimer's.

The direct and indirect costs of caring for individuals with the disease is estimated at $100 billion annual.

By 2030, when the baby boom generation is over 65, it is estimated that the number of people with Alzheimer's will soar to levels exceeding the country's ability to treat them or absorb those costs.

"If you can delay Alzheimer's for five years you can reduce in half the number of people with it,'' Bernick said. "You don't even have to cure it. You just have to have something that can stop its progression.''

Samaritan Pharmaceuticals' lab is in Maryland, but its Las Vegas office handles patents and licensing of drugs developed by the company, Greeson said.

Samaritan develops drugs for the treatment of AIDS, Alzheimer's, cancer and heart disease, Greeson said.

In terms of what this means for Nevadans, Bernick said it fits into the general strategic plan of health sciences development in the state.

"With the Nevada Cancer Institute and the Lou Ruvo Institute and the academic health sciences center that is being pitched, all these things are kind of jelling now,'' he said.

"And, I think with Samaritan being here, it shows that Las Vegas and Nevada are becoming more than just a town for hospitality and gaming. There is science going on and because of that, people are going to receive top care.''



<small>Find this article at:
http://www.reviewjournal.com/lvrj_home/ ... 02552.html </small>

[palmspringsbum]

Joan Bakewell: Alzheimer's research can no longer be sidelined

The Independent
Friday, 14 March 2008


It's good news for Terry Pratchett, Britain's highest-profile Alzheimer's sufferer. Alzheimer's syndrome is a disease of old age that could lie in wait for any of us and sometimes ambushes those who think of themselves as merely middle aged. Terry Pratchett is 59. The good news is that research is showing that cannabis slows down memory loss. The recent report from the Hebrew University of Jerusalem, has involved mice, but is now moving towards human trials.


This won't come as a surprise to America's Drug Watch Oregon, whose Marijuana Research Review has been publishing for decades the many investigations and tests going forward on marijuana. With 400 chemicals present in the plant it's hardly surprising it has diverse, sometimes contradictory, effects. Many of the Review's findings have come with substantial warnings that the ever-stronger forms of the drug common in the 1990s, carry a whole variety of risks: adverse effect on the immune system; interference with the capacity to control body heat; short-term memory loss; and an impaired ability to learn.

Reports also found that smoking marijuana enhanced abnormalities in some multiple sclerosis patients. So this latest news is by no means a call to return to the weed by those for whom 50 years ago it was simply part of a free-wheeling lifestyle. There is an irony, though, in the thought that those same independent spirits now in their sixties may be needing it for an altogether more serious condition.

The fact is the Oregon Health Division has just expanded the state's medical programme by adding Alzheimer's disease to those conditions that qualify for state-sanctioned marijuana use. Their 1998 initiative already allows it in cases of cancer, glaucoma, HIV/Aids, severe nausea, seizures, and persistent muscle spasms.

But Oregon is not expecting a rush. A representative from among Oregon's 60,000 Alzheimer's patients calls for "an extensive scientific study... to examine both positive and negative effects". "That clearly has not happened yet, and we really cannot endorse it at this point," he said. The good news for Terry Pratchett is that work is going forward steadily to find a treatment.

For me, the fear of losing my memory is even more haunting than the prospect of death. The older I get the more I realise I am defined by all that I have done and known, and when memories begin to thin out, something intrinsic to my sense of identity goes too. We can't recall everything that's happened: the brain would choke on its own superabundance.

And there is no doubt some peace of mind to be gained in repressing traumatic and damaging occasions. I have always been suspicious of those talking cures that insist on retrieving long-dormant pain and suffering. But old age is made up of memories and living with them is saner than living without them.

I sat with friends recently thumbing through old photograph albums in which we all figured. Each of us remembered different faces and circumstances. Each had forgotten different things. That is part of being old. And incidentally the final use for all those accumulating heaps of old snaps. Forgetfulness shades only gradually into memory-loss. The daily trivia begins to recur more often: where did we leave the keys, what did I come upstairs to fetch, have I told this anecdote to you before? Long before... or half an hour ago?

So worry creeps up on us, wondering how soon to ask the doctor, go for tests. The British are more reticent than the Germans who apparently turn up early and are put on appropriate drugs sooner. Old people fear making a fuss, and are so often treated with casual disregard by society that they simply shut up and put up. This won't do any longer.

The government spends on Alzheimer's research a mere 3 per cent of what it spends on cancer. Given the demographic trends that predict a steady rise in the proportions of us over 50, Alzheimer's deserves a higher priority. Pratchett has been afflicted for two and a half years: he has just finished his latest novel and begun the next. He believes that in future a combination of lifestyle and drugs may hold back the development of his Alzheimer's into the seriously disabling dementia we all fear.

Alzheimer's is a private ailment and a private dread. How many of us have aged parents drifting silently into a world of unknowing. But with people like Pratchett speaking out and scientific researches making the headlines the Government must be left in no doubt that this is an issue with a growing constituency. They must not let it slip their memory!

joan.bakewell@virgin.net