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New Finding Could Mark Shift in Alzheimer's Research
Date:4/29/2010

'Floating' clumps of protein, not plaques, may cause the disease, researchers say

THURSDAY, April 29 (HealthDay News) -- New research could change the way scientists view the causes -- and potential prevention and treatment -- of Alzheimer's disease.

A study published online this month in the Annals of Neurology suggests that "floating" clumps of amyloid beta (abeta) proteins called oligomers could be a prime cause of the disorder, and that the better-known and more stationary amyloid-beta plaques are only a late manifestation of the disease.

"Based on these and other studies, I think that one could now fairly revise the 'amyloid hypothesis' to the 'abeta oligomer hypothesis,'" said lead researcher Dr. Sam Gandy, a professor of neurology and psychiatry and associate director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York City.

The new study could herald a major shift in Alzheimer's research, another expert said.

Maria Carrillo, senior director of medical and scientific relations at the Alzheimer's Association, said that "we are excited about the paper. We think it has some very interesting results and has potential for moving us in another direction for future research."

According to the Alzheimer's Association, more than 5.3 million Americans now suffer from the neurodegenerative illness, and it is the seventh leading cause of death. There is no effective treatment for Alzheimer's, and its origins remain unknown. For decades, research has focused on a buildup of amyloid beta plaques in the brain, but whether these deposits are a cause of the disease or merely a neutral artifact has remained unclear.

The new study looked at a lesser-known factor, the more mobile abeta oligomers that can form in brain tissue. In their research, Gandy's team first developed mice that only form abeta oligomers in their brains, and not amyloid plaques.<
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