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Genentech Offers New Theory For Alzheimer's

Posted by Chrissie Cole
Thursday, February 19, 2009 2:01 PM EST
Category: Major Medical
Tags: FDA and Prescription Drugs, Alzheimer's Disease, Dementia, Memory Loss, Genentech Inc.


IMAGE SOURCE: Genentech Inc.

Alzheimer’s disease has been one of medicine’s biggest mysteries, but U.S. scientists have a new theory which may pave the way for potential new treatments.

Current drugs delay the symptoms of Alzheimer’s, but there is no cure. Alzheimer’s is the sixth leading cause of death in the United States. An estimated 5.2 Americans are currently living with the disease.

A new study, published in the journal Nature, by researchers at Genentech Inc., suggests a new mechanism of nerve-cell death may lead to brain deterioration in Alzheimer’s disease.

The research focuses on amyloid precursor protein or APP for short. For some time researchers have known that APP is a bad actor in Alzheimer’s disease, but until now they have been unsure how it participates,” said Marc Tessier-Lavigne, senior vice president, Research Drug Discovery at Genentech.

Two components of APP appear to cause nerve cells to self-destruct: the amyloid beta peptide, which collects abnormal plaques in the brain are a diagnostic size of Alzheimer’s and the N fragment, called N-APP for short, can trigger a chain of events that destroys neurons, according to the study.

“The findings are expected to have a major impact on Alzheimer’s research,” said Paul Greengard, of Rockefeller University, in New York, who has received a Nobel Prize for his work on nerve cell communication.

While more research is needed as the study is based on laboratory and rodent experiments, if the same mechanism is found to be true in humans, the discovery may lead to new targets for drug development to slow degenerative brain diseases, Tessier-Lavigne said.

Several drug companies are working on new drugs to remove beta amyloid from the brain, but few have had success in altering the course of the disease.

Next researchers intend to see if the same mechanism holds true in adult brain cells. The question then becomes, can they interfere with and halt the progression of Alzheimer’s disease? #

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