Salk Institute for Biological Studies: InsideSalk

Delaying the Aging Process Protects Against Alzheimer's Disease

Aging is the single greatest risk factor for Alzheimer's disease. In their latest study,researchers led by Andrew Dillin, associate professor in the Salk Institute Molecular and Cell Biology Laboratory, found that simply slowing the aging process in mice prone to develop Alzheimer's disease prevented their brains from turning into a neuronal wasteland.

Published in Cell, their finding is the latest clue in Salk scientists' 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.

"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.

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, which plays a crucial role in the regulation of lifespan and youthfulness across many species. As a result, mice with reduced IGF-1 signaling lived up to 35 percent longer than normal mice.

Cohen then employed a battery of behavioral tests and concluded that 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.

"Our study opens up a whole new avenue of looking at the disease," says Dillin, a Howard Hughes Medical Investigator. "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.

"This work is a celebration for the entire field of aging researchers, as it validates the long-held hypothesis that genetic and pharmacologic changes to create a healthy lifespan, or 'healthspan,' can greatly reduce the onset of some of the most devastating diseases that afflict mankind," he adds.


InsideSalk 02|10 Issue | © Salk Institute for Biological Studies