Publication date: Jul 25, 2019
This post was originally published on this site Differences in the activity of a protein called Cdk5 in the brain could be a cause of – and perhaps even a target for the treatment of – depression related to Huntington’s disease, research in mice suggests. In analyzing the mice’s brains, the researchers found that Cdk5 activity was higher in the nucleus accumbens and the prefrontal cortex – two regions of the brain associated with, among other things, depression. For example, the mice treated with the Cdk5 blocker were quicker to move in stress tests than mice given a placebo – although it should be noted that the treated mice with Huntington’s still showed more depression-like symptoms than mice without the disease. Importantly, when the researchers engineered Huntington’s mice with a version of DARPP-32 that could no longer be phosphorylated by Cdk5, the mice no longer had depression-like symptoms. These data suggest that preventing this specific molecular event – the phosphorylation of DARPP-32 by Cdk5 – could be a feasible strategy for preventing and treating depression in people with Huntington’s.
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