Alzheimer's disease is usually accepted as a hazard of aging, but researchers actually do not know whether neurodegenerative diseases are a consequence of aging// or not. Researchers at the Salk Institute for Biological Studies and the Scripps Research Institute have now conducted a study that proves it is aging that is critical for diseases like Alzheimer's.
Harmful beta amyloid aggregates accumulate when aging impedes two molecular clean-up crews from getting rid of these toxic species.
This finding opens the door for development of drugs preventing build-up of toxic protein aggregates in the brain. The study appears in the Aug. 10 issue of Science Express, the advanced online edition of the journal Science.
"Aging is the most important risk factor for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease," says senior author Andrew Dillin, Ph.D., an assistant professor in the Salk Molecular and Cell Biology Laboratory. "Our study revealed that the age onset of these diseases is not simply a matter of time but that the aging process plays an active role in controlling the onset of toxicity," he explains.
Beta amyloid production occurs in all brains, but healthy cells clear away excess amounts. Brains of people with Alzheimer's disease, on the other hand, are unable to control beta amyloid accumulation. For years, scientists have scrambled to find out why.
To answer this vexing question, Dillin analyzed protein aggregation in the roundworm, a streamlined organism that, like mammals, uses the insulin/IGF-1 pathway to control lifespan but can be rapidly manipulated genetically. Dillin used roundworms that produce human beta amyloid peptide in body wall muscles. As the worms aged, the protein formed toxic aggregates causing paralysis.
Then researchers experimentally decelerated aging in engineered worms by lowering activity of the insulin/IGF-1 patPage: 1 2 3 Related medicine news :1
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