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Fasting forestalls Huntington's disease in mice

Decreasing meal frequency and caloric intake protects nerve cells from genetically induced damage, delays the onset of Huntington's disease-like symptoms in mice, and prolongs the lives of affected rodents, according to investigators at the National Institute on Aging (NIA) Intramural Research Program. This animal study* is the first to suggest that a change in diet can influence the course of Huntington's disease.

"If reducing food intake has the same effects in humans as it does in mice, then it may be theoretically possible to delay the onset of the disease and extend the lives of Huntington's patients by prescribing low-caloric diets or diets with reduced meal frequency," says Mark Mattson, Ph.D., chief of the NIA's Laboratory of Neurosciences. The study will be published in the Proceedings of the National Academy of Sciences Online Early Edition the week of February 10 (doi:10.1073/pnas.0536856100).

In the study, NIA scientists found that when mutant huntingtin, the abnormal human gene that causes Huntington's disease (HD), was introduced into mice, these mice exhibited clinical signs of the disease, including abnormal metabolism. This altered metabolism, a diabetes-like condition also found in humans with HD, caused the mice to progressively lose weight despite having good appetites. As the mice aged, they developed difficulties controlling their body movements, lost body weight, and eventually died. When the NIA investigators examined the brains of these mice, they discovered that nerve cells in the striatum, a brain region that normally helps control body movements, had degenerated, just like human nerve cells affected by HD. Previously, Dr. Mattson found that reducing the food intake of rats and mice by maintaining them on low-calorie diets or by intermittent fasting--depriving the animals of food for a 24-hour period every other day--can improve glucose metabolism and can protect brain nerve cells in experimental models of Parkinson's disease
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Contact: Doug Dollemore
dollemod@nia.nih.gov
301-496-1752
NIH/National Institute on Aging
10-Feb-2003


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