The way we age have impact on the prevention of Alzheimer's disease

( aging is the greatest risk factor )

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Aging is the single greatest risk factor for Alzheimer's disease. In their latest study, researchers at the Salk Institute for Biological Studies found that simply slowing the aging process in mice prone to develop Alzheimer's disease prevented their brains from turning into a neuronal wasteland.
"Our study opens up a whole new avenue of looking at the disease," says the study's leader, Howard Hughes Medical Investigator Andrew Dillin, Ph.D., a professor in the Salk Molecular and Cell Biology Laboratory. "Going forward, looking at the way we age may actually have more impact on the treatment and prevention of Alzheimer's disease than studying the basic biology of the disease itself."
Their finding, published in the Dec. 11, 2009 issue of the journal Cell, is the latest clue in the Salk scientists' ongoing quest to shed light on the question of whether Alzheimer's disease onset late in life is a disastrous consequence of the aging process itself or whether the beta amyloid aggregates that cause the disease simply take a long time to form.
Age is the major risk factor for the development of Alzheimer's disease. Beyond age 65, the number of people with the disease doubles every five years. Centenarians, however, seem to escape most common age-related diseases, including the ravages of Alzheimer's disease. "In this study, we went directly to the root cause of Alzheimer's disease and asked whether we could influence the onset of the disease by modulating the aging process," says first author Ehud Cohen, Ph.D., formerly a postdoctoral researcher in Dillin's lab and now an assistant professor at the Hebrew University-Hadassah Medical School in Jerusalem, Israel.
To answer this intriguing question, he slowed the aging process in a mouse model for Alzheimer's by lowering the activity of the IGF-1 signaling pathway. "This highly conserved pathway plays a crucial role in the regulation of lifespan and youthfulness across many species, including worms, flies, and mice and is linked to extreme longevity in humans," he explains. As a result, mice with reduced IGF-1 signaling live up to 35 percent longer than normal mice. Cohen then employed a battery of behavioral tests to find out whether it was simply the passage of time or aging per se that determined the onset of the disease. Chronologically old but biologically young animals appeared nearly normal long after age-matched, normal-aging Alzheimer's mice exhibited severe impairments in their ability to find a submerged platform in the Morris water maze or stay atop a revolving Rota Rod. ...http://www.physorg.com

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