Delay aging process to guard against Alzheimer’s disease. The way we age may have a greater impact on treatment and prevention of Alzheimer’s than studying basic biology of the disease. | Home Care Assistance Delay aging process to guard against Alzheimer’s disease. The way we age may have a greater impact on treatment and prevention of Alzheimer's than studying basic biology of the disease. | Home Care Assistance
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Delay aging process to guard against Alzheimer’s disease. The way we age may have a greater impact on treatment and prevention of Alzheimer’s than studying basic biology of the disease.

-Dr. Kathy Johnson, PhD, CMC

Most senior citizens try to resist aging. Aging it looks like is the single greatest risk factor for Alzheimer’s disease. Researchers at the Salk Institute for Biological Studies in a study released this month found that simply slowing the aging process in mice which are prone to develop Alzheimer’s disease prevented their brains from turning into a neuronal wasteland.

Howard Hughes Medical Investigator Andrew Dillin, Ph.D., a professor in the Salk Molecular and Cell Biology Laboratory, the lead researcher believes that this finding opens up a whole new avenue of looking at the disease. This finding was published in the Dec. 11, 2009 issue of the journal Cell. It is the latest clue in the 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 said to be the major risk factor for the development of Alzheimer’s disease. The number of people with the disease beyond the age of 65 doubles every five years. However, centenarians seem to escape most common age-related diseases, including the ravages of Alzheimer’s disease.

This study went directly to the root cause of Alzheimer’s disease to find whether the onset of the disease could be influenced by modulating the aging process. To answer this question, 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, the aging process in a mouse model for Alzheimer’s by lowering the activity of the IGF-1 signaling pathway. Such a conserved pathway plays a crucial role in the regulation of lifespan and youthfulness across many species and is linked to extreme longevity in humans. As a result, mice with reduced IGF-1 signaling are able to live up to 35 percent longer than normal mice.

A battery of behavioral tests was employed to find out whether it was simply the passage of time or aging per se that determined the onset of the disease. It was found 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 task or stay atop a revolving Rota Rod.

Such behavioral differences between normal and long-lived mice became apparent at nine months of age. The big surprise came when the plaques in their brains were studied closely. The buildup of toxic clumps of beta amyloid plaques in the brain is one of the telltale signs of Alzheimer’s disease.

The production of beta amyloid probably occurs in all brains, but healthy cells clear away excess amounts. Brains of people with Alzheimer’s disease have been found to have an inability to control beta amyloid accumulation. This was found true for Alzheimer’s mouse models, which are genetically engineered to overproduce beta amyloid.

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

Previously it was thought that plaques are the causative agents of Alzheimer’s disease. But the results of this study support the emerging theme that they have a protective function. Mice become less efficient at stowing away toxic beta amyloid fibrils in tightly packed aggregates as they age.

In an earlier study Cohen et al used roundworms to study the effects of the aging process on protein aggregation. They found that high molecular weight aggregates of beta amyloid might actually be less toxic than smaller beta amyloid fibrils. But whether these results would be relevant for mammals cannot be ascertained as worms don’t have brains as we do.

Three studies found that some very long-lived humans carry mutations in components of the IGF-1 signal pathway. The same pathway was perturbed to increase the lifespan of the mice in the study. This work serves as an impetus as it validates the long-held hypothesis that genetic and pharmacologic changes to create a healthy lifespan, or ‘health span,’ can greatly reduce the onset of some of the most devastating diseases that afflict mankind.

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