Tuesday, September 7, 2010

New Research Regarding Alzheimer's & DS

A recent study was published in regards to the Amyloid Beta Protein and it's role in both Alzheimer's disease and Down syndrome. This protein is overexpressed in DS and is also responsible for the plaques and tangles which forms in AD patients.

This is one hope of Longvida Curcumin, to break up the plaques and tangles caused by APP. Curcumin is known to break up those plaques and tangles, but from what it appears it needs to be a very high dose. So, that is still in the works.

But what this study researched was what enzyme causes APP to produce plaques and tangles and a means to control that. While no drug or therapy that is safe has been found yet, this is non-the-less very interesting and noteworthy.

To see the abstract of the study, click here.

By Dr Cesar Chelala /New York

A finding by a team of Rockefeller University scientists led by Dr Paul Greengard, a Nobel laureate, throws light on an important feature of Alzheimer’s disease. The finding may result in better treatment for both this disease and for patients with Down syndrome. Better treatment for both diseases could improve the lives of millions of people worldwide.

Patients with both Alzheimer’s disease and with Down syndrome have an accumulation of a protein called beta-amyloid in their brains. The accumulation of this substance is believed to initiate the pathological changes (among them the plaque that builds up in the brains of people with Alzheimer’s) leading to brain dysfunction, cell death and dementia. The hallmark lesions (tangles and plaques) of Alzheimer’s disease are also present in all adults with Down syndrome after the age of 40, suggesting a shared genetic susceptibility to both.

Although it wasn’t known if beta-amyloid played a role in mental retardation, particularly in Down syndrome patients, the Rockefeller scientists worked under the hypothesis that it could have an effect. If this were true, they reasoned, lowering levels of beta-amyloid could result in an improvement of symptoms.

Dr Greengard and his collaborators found an enzyme (enzymes are proteins that speed up chemical reactions) that stimulates the production of beta-amyloid. In the new study, led by Gen He, a research associate in Greengard’s lab, the researchers showed that the enzyme stimulates production of beta-amyloid in cell lines, and that reducing it brings down beta-amyloid. That enzyme could thus be an important target for the development of new drugs against Alzheimer’s disease.

To test the hypothesis that increased beta-amyloid could be responsible for the symptoms of mental retardation, Dr Greengard and his colleagues tested a compound which is known to suppress the production of beta-amyloid in a mouse model with Down syndrome. Mice treated with this compound not only had a rapid reduction of beta-amyloid but also showed a significant improvement in their ability to learn to navigate a water maze. They were also able show some other signs of improved mental functioning. The control group used did not show any of these effects.

In another set of experiments, Dr Greengard and his colleagues developed a strain of mice that had a gene for Alzheimer’s. When they blocked the gene for the enzyme that increases the production of beta-amyloid, the animals didn’t develop plaque in their brains.

Reality in science is always more complex than anticipated, though. The compounds used to lower the levels of beta-amyloid have generally some serious toxic side effects. Only one of these compounds, the anti-cancer drug Gleevec, used to treat a rare form of leukaemia, was able to lower beta-amyloid without toxic side effects. The problem with Gleevec, though, is that it doesn’t remain in the brain long enough to treat either Alzheimer’s disease or Down syndrome. The importance of Gleevec, according to Dr Greengard, is that it may provide a model for developing new anti-beta-amyloid drugs.

The discovery of a new target for these drugs is a new and significant development in the treatment of Alzheimer’s disease and Down syndrome, both of which affect millions of people worldwide.  Only in the US, it is estimated that approximately 4mn Americans are affected by Alzheimer’s disease.

In what until recently had been an almost hopeless situation, the discoveries of Dr Paul Greengard and his colleagues shed a new light into what had been until now a rather dismal situation.



Kent said...

We at the Fisher Center for Alzheimer’s Research Foundation are very proud to have funded this tremendous new finding of Dr. Paul Greengard. For the past 15 years, we have been proud to support the good work of Dr. Greengard and his internationally renowned team of scientists at The Fisher Center for Alzheimer’s Disease Research. We would like to specifically congratulate Drs. He and Greengard for discovering this important protein. Their latest research is a potential paradigm shift in how scientists and doctors around the world will attack Alzheimer’s.
Kent L. Karosen
President and CEO Fisher Center for Alzheimer’s Research Foundation

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