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Delaying Aging Process May Prevent Alzheimer's

If getting old is the greatest risk factor for developing Alzheimer's disease, then slowing the aging process just might prevent the dreaded, incurable disease.

Researchers at the Salk Institute for Biological Studies, in La Jolla, California, followed that line of reasoning and 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," said the study's leader, 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 journal Cell, is the latest clue in the Salk scientists' ongoing quest to shed light on the question of whether Alzheimer's onset late in life is a disastrous consequence of the aging process itself or whether the beta amyloid that causes 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.

 

"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," said 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 said.

 

As a result, mice with reduced IGF-1 signaling live up to 35% 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.

 

One of the telltale signs of Alzheimer's disease is the buildup of toxic clumps of beta amyloid plaques in the brain. Beta amyloid production probably 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. The same is true for Alzheimer's mouse models, which are genetically engineered to overproduce beta amyloid.

 

Although long-lived mice didn't show any of the cognitive or behavioral impairments typical of Alzheimer’s disease until very late in life, their brains were riddled with highly compacted plaques.

 

"Although before it was thought that plaques are the causative agents of Alzheimer's disease, our results clearly support the emerging theme that they have a protective function," said Cohen. "As mice age, they become less efficient at stowing away toxic beta amyloid fibrils in tightly packed aggregates."

 

What have the scientists learned from this study? That staying active and healthy throughout a lifespan, especially late in life, can in fact reduce the risk of developing devastating diseases in old age. More research is planned.

 

(Article courtesy of ConsumerAffairs.com)

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