( A new study appearing in the January 18...)Dividing Nerve Cells Could Trigger Alzheimer's Disease,Health

A new study appearing in the January 18 issue of The Journal of Neuroscience, says that Alzheimer's disease (AD) could be triggered off when adult neurons try to undergo division. This finding in laboratory// mice could help scientists understand the mechanism behind the development of the disease.

"If you could stop cell cycling, you might be able to stop neurons from dying prematurely. This could be a fresh approach to therapy for Alzheimer's and other diseases, including stroke, amyotrophic lateral sclerosis [also known as Lou Gehrig's disease], and HIV dementia," said lead researcher Karl Herrup, Ph.D., of Case Western Reserve University in Cleveland. Neurons affected by Alzheimer's and other degenerative disease start to divide before they die. This cell division starts before the amyloid plaques that are distinctive to the disease start to appear. In the current study, researchers compared three different mouse models of AD to the brains of normal mice. They found that in the AD models, proteins related to cell cycle started appearing before amyloid plaques. Many of the neurons had increased chromosome number. The cortex and the hippocampus regions were the most affected in the lab mice. These are the same areas that are affected by AD. "The cell cycle markers mimic the human situation rather well," said Dr. Herrup. "This opens a range of new experimental possibilities using the cell cycle events as indicators of neuronal distress." His team is now working towards finding out if Ibuprofen can stop this neurodegenaration. Ibuprofen is a NSAID that decreases the production of amyloid beta and some studies have indicated that it could be beneficial in AD. This study was partly funded by National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

Original Article: YangY, Varvel NH, Lamb BT, Herrup K. Ectopic cell cycle events link human Alzheimer's disease and APP transgenic mouse models. The J
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