Gleevec Reverses Alzheimer's Plaques in Mice

There is quite a bit of new information here, but the big one is that a cancer drug Gleevec is able to directly reduce the amount of amyloid in the brain quickly.

In fact it appears to massively reverse the problem in quick time which allows us to limit side effects from the drug itself.

It is reasonable to suppose such a reduction would allow the brain to substantially heal from the insult.

Again this is early days, but it seems that a quick check on Gleevec users who also suffered from symptoms of Alzheimer’s need to be investigated to see if improvements were observed in any form.

If we are lucky, we finally have a simple treatment that effectively reverses the process and at least halts the disease.

Gleevec treatment reduces amyloid plaque in mice brains and half of Alzheimers cases are preventable through lifestyle change and preventing chronic conditions

JULY 25, 2011

http://nextbigfuture.com/2011/07/gleevec-treatment-reduces-amyloid.html

1. The plaques associated with Alzheimer’s disease may arise in the liver, not the brain as commonly thought, according to a study published in The Journal of Neuroscience.

Researchers found that three genes that protected mice against plaque deposition in neurons were correlated with expression of the genes in the liver, where the plaques are also produced. However, there was no such correlation between the activity of the genes in the brain and plaque deposition there.

Mice were given the cancer drug Gleevec, which reduces production of beta amyloid plaques. Gleevec treatment greatly reduced beta amyloid levels in the mice, including the brain.

“In a week, that reduced the amount of amyloid in the brain by 50 percent,” Sutcliffe said. “We know that about a 20 percent increase in amyloid in mice will cause them to develop Alzheimer’s disease-like symptoms. 50 percent is a whopping reduction.”

Apparently Novartis will not fund the research and clinical trials for applying Gleevec to Alzheimer's. Scripps is fundraising to pay for the clinical trials.

Peripheral reduction of β-amyloid is sufficient to reduce brain β-amyloid: Implications for Alzheimer's disease

2. Over half of all Alzheimer’s disease cases could potentially be prevented through lifestyle changes and treatment or prevention of chronic medical conditions, according to a study led by Deborah Barnes, PhD, a mental health researcher at the San Francisco VA Medical Center (SFVAMC).

In the United States, Barnes found that the biggest modifiable risk factors are physical inactivity, depression, smoking, mid-life hypertension, mid-life obesity, low education and diabetes.

Together, these risk factors are associated with up to 51 percent of Alzheimer’s cases worldwide (17.2 million cases) and up to 54 percent of Alzheimer’s cases in the United States (2.9 million cases), according to Barnes.

“What’s exciting is that this suggests that some very simple lifestyle changes, such as increasing physical activity and quitting smoking, could have a tremendous impact on preventing Alzheimer’s and other dementias in the United States and worldwide,” said Barnes, who is also an associate professor of psychiatry at the University of California, San Francisco (UCSF).

The study results were presented at the 2011 meeting of the Alzheimer’s Association International Conference on Alzheimer’s Disease in Paris, France, and published online on July 19, 2011 in Lancet Neurology.

Barnes cautioned that her conclusions are based on the assumption that there is a causal association between each risk factor and Alzheimer’s disease. “We are assuming that when you change the risk factor, then you change the risk,” Barnes said. “What we need to do now is figure out whether that assumption is correct.”

3. Discovery Magazine - the environmental toxin beta-methylamino-L-alanine, or BMAA may be an important factor for Alzheimer's and Parkisons. 

This compound 
is produced by cyanobacteria, the blue-green algae that live in soil, lakes, and oceans. Cyanobacteria are consumed by fish and other aquatic creatures. Recent studies have found BMAA in seafood, suggesting that certain diets and locations may put people at particular risk. More worrisome, blooms of cyanobacteria are becoming increasingly common, fueling fears that their toxic by-product may be quietly fomenting an upsurge in ALS—and possibly other neurological disorders like Alzheimer’s disease and Parkinson’s as well. 21 research teams from 11 countries are now investigating the potential dangers of BMAA.

The data suggest that ALS is 2.5 times more common than average within one-half mile of a lake or pond where cyanobacteria have bloomed. Stommel hypothesizes that people living around the lakes may have breathed in BMAA from the air, eaten fish contaminated with it, or accidentally swallowed it 
while swimming. He and Cox are conducting tests of brain bank tissue to see if the ALS patients in these regions do in fact have elevated levels of BMAA.

The overall risk from BMAA is probably low. In fact, he eats shrimp and crab with relish. “ALS is very rare, and only a few people are genetically at risk,” he says. “Even if BMAA causes common disorders like Alzheimer’s and Parkinson’s, that still doesn’t mean we should shun seafood.” Commercial fishermen generally are not working in areas heavily contaminated with cyanobacteria, he notes, so the danger of exposure in the United States and Canada should be modest for those who eat typical store-bought or homegrown food and avoid drinking—as Cox puts it—“green, smelly” water.