A new study in mice suggests that Alzheimers disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it. The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and appears in the January 18, 2006 issue of The Journal of Neuroscience.*
For unknown reasons, nerve cells (neurons) affected by AD and many other neurodegenerative diseases often start to divide before they die. The new study shows that, in animal models of AD, this abnormal cell division starts long before amyloid plaques or other markers of the disease appear. Cell division occurs through a process called the cell cycle. "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 Alzheimers and other diseases, including stroke, amyotrophic lateral sclerosis [also known as Lou Gehrigs disease], and HIV dementia," says Karl Herrup, Ph.D., of Case Western Reserve University in Cleveland, who led the study.
The researchers compared the brains of three different mouse models of AD to brains from normal mice, looking specifically for markers of cell cycling. They found that, in the AD mouse models, cell cycle-related proteins appeared in neurons 6 months before the first amyloid plaques or disease-related immune reactions developed in the brain. Many of the neurons also had increased numbers of chromosomes, which is typical of cells that have begun to divide. These changes were not seen in normal mice. The regions of the brain most affected by the neuronal cell cycling were the cortex and the hippocampus – the same regions most affected in AD. The cortex is important for thought and reasoning, while the hippocampus plays a key role in learning and memory. Some parts of the brainstem also showed evidence of cell cycling.
Natalie Frazin | EurekAlert!
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