Monday, 19 August 2013

New target inhibiting the progression of Alzheimer's disease

Main Category: Alzheimer's / Dementia
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
New target inhibiting the progression of Alzheimer's disease
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To stop the progression of Alzheimer's disease in the early stage, it is necessary to identify new therapeutic targets.

Prof. Yunpeng Cao and team from the First Affiliated Hospital of China Medical University examined striatal-enriched phosphatase 61 expression in the brain tissues of Alzheimer's disease rats using in vivo and in vitro models, and analyzed the molecular mechanism by which striatal-enriched phosphatase 61 regulates N-methyl-D- aspartate receptor 2B transport.

The researchers found that valeric acid (AP5), an N-methyl-D-aspartate receptor antagonist, significantly inhibited amyloid- beta 1-induced increased activity of striatal-enriched phosphatase 61. In addition, the phos-phorylation of N-methyl-D-aspartate receptor 2B at Tyr1472 was impaired in amyloid-beta 1-treated cortical neurons, but knockdown of striatal-enriched phosphatase 61 enhanced the phosphorylation of N-methyl-D-aspartate receptor 2B.

Collectively, these findings, published in Neural Regeneration Research (Vol. 8, No. 21, 2013), indicate that striatal-enriched phosphatase 61 can disturb N-methyl-D-aspartate receptor transport and inhibit the progression of learning and study disturbances induced by Alzheimer's disease. Thus, striatal-enriched phosphatase 61 may represent a new target for inhibiting the progression of Alzheimer's disease.

Article: " What is the new target inhibiting the progression of Alzheimer's disease?," by Lin Zhang1, Jing Yang2, Yunpeng Cao1 (1 Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China; 2 Provincial Key Laboratory of Cardiovascular and Cerebrovascular Drug Basic Research, Liaoning Medical University, Jinzhou 121001, Liaoning Province, China). Neural Regen Res. 2013;8(21):1938-1947. doi:10.3969/j.issn.1673-5374.2013.21.002

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