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Excess Cdk5 Enzyme Can Harm Brain

by Medindia Content Team on  December 8, 2005 at 5:01 PM Research News   - G J E 4
Excess Cdk5 Enzyme Can Harm Brain
A research conducted by the Howard Hughes Medical Institute, the National Institute of Mental Health and the Harvard Medical School has revealed that a brain enzyme plays a prominent role in maintaining and developing learning and memory. If the enzyme is present in high levels, then it can have adverse effects on the brain. The tests were conducted on mice. The Cdk5 enzyme also plays an important role in the death of neurons in disorders like the Alzheimer's disease.
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According to the researchers' studies, increased levels of Cdk5, as well as increased levels of a regulatory protein called p25 that is known to hyper-activate Cdk5, had been found in the brains of patients suffering from Alzheimer's. In the study, the researchers used mice in which they could switch on p25 at will in the brain's learning and memory center, the hippocampus. It was found that while in the mice in which p25 was switched on for only two weeks, actually enhanced learning and memory, in contrast, mice in which p25 had been switched on for six weeks showed impaired learning and memory in certain tasks.

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The researchers said that this indicated that elevated levels of p25 impaired learning and memory. This indicates that transient p25 production facilitated learning, whereas the ability to form new memories was impaired by prolonged p25 expression, according to the researchers said. The study showed that it was possible that chronic exposure to Alzheimer's risk factors would increase the p25 to a level that would contribute to neural loss.

The researchers said that the increase in p25 levels might be a mechanism to compensate for the damage from such diseases like Alzheimer's. This may cause the enzyme, whose work it was to stop degeneration, actually quicken the process. The evidence that is provided by the study is that the p25 generation might be a compensatory phenomenon to enhance neuroplasticity. These mice may also serve as a model whereby a factor that promotes plasticity can eventually contribute to neurodegeneration according to the researchers. (ANI)
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