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Blood Sugar Linked to Aging Brain

December 30, 2008

December 30, 2008

Keeping blood sugar in check is not just a key to preventing diabetes. It may also help to keep the brain sharp into old age.

Those are the findings of a new study from researchers at Columbia University Medical Center in New York. They found that maintaining blood sugar levels as we age may be key to preserving memory and mental function. While abnormal regulation of blood sugar, or glucose, levels are normally associated with diabetes, the new findings suggest that normal regulation of blood sugar is  also critical for brain health. The study appeared in the December issue of the medical journal Annals of Neurology.

Most people experience “senior moments” as they age, periods when they might forget a friend’s name or where they placed the car keys. The lapses are by no means as serious as those that occur with Alzheimer’s disease, but they can be distressing. They are also often considered a normal part of aging.

The new findings suggest that rising blood sugar levels, a precursor of diabetes, are responsible in part for these lapses in memory. Regular exercise to help maintain steady blood sugar levels, a key component of diabetes management, may be a way to help ward off memory declines with age.

“This is news even for people without diabetes, since blood glucose levels tend to rise as we grow older,” reported lead investigator Dr. Scott A. Small, M.D., an Alzheimer’s researcher at Columbia University. “Whether through physical exercise, diet or drugs, our research suggests that improving glucose metabolism could help some of us avert the cognitive slide that occurs in many of us as we age.”

Using brain scans of people, monkeys and mice, the new research looked at a part of the brain called the hippocampus, a seahorse-shaped section that is critical for memory and learning. It has long been known that the early stages of Alzheimer’s disease cause damage to the hippocampus, and studies have suggested that it is also vulnerable to the effects of normal aging. But until now, the underlying causes of age-related hippocampal damage have remained largely unknown.

The study looked at measures that typically change during aging, like rising blood sugar and insulin levels, and rising levels of obesity and cholesterol. The researchers found that of all these components, rising levels of blood glucose were the only factor that was closely tied to decreasing activity in a memory-critical part of the hippocampus called the dentate gyrus.

“Beyond the obvious conclusion that preventing late-life disease would benefit the aging hippocampus, our findings suggest that maintaining blood sugar levels, even in the absence of diabetes, could help maintain aspects of cognitive health,” Dr. Small said. “More specifically, our findings predict that any intervention that causes a decrease in blood glucose should increase dentate gyrus function and would therefore be cognitively beneficial.”

The new findings also suggest that physical activity may be good for the aging brain, because exercise has been shown to help preserve activity in the dentate gyrus. “By improving glucose metabolism, physical exercise also reduces blood glucose,” Dr. Small explained. “Improving glucose metabolism could be a clinically viable approach for improving the cognitive slide that occurs in many of us as we age.”

Other studies likewise support the link between blood sugar, diabetes and Alzheimer’s disease. A long-term study of men in Sweden, for example, found that men who develop diabetes in mid-life are at significantly increased risk of getting Alzheimer’s disease in old age. [See the ALZinfo.org study, “Diabetes in Mid-life Increases Alzheimer’s Risk,”] Diabetes has also been linked to mild cognitive impairment, a form of memory loss that may precede Alzheimer’s disease. [See the ALZinfo.org story, “Diabetes Linked to Memory Problems,”]

By www.ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Annals of Neurology, December 2008.

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