《Chinese Journal of Rehabilitation Theory and Practice》 ›› 2020, Vol. 26 ›› Issue (10): 1182-1185.doi: 10.3969/j.issn.1006-9771.2020.10.010

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Advance in Mechanisms of Calpain Involved in Hyperphosphorylation and Truncation of Tau Protein (review)

GUO Kai-wen,YANG Cui-cui,ZHANG Lan()   

  1. Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing 100053, China
  • Received:2019-08-14 Revised:2019-12-23 Published:2020-10-25 Online:2020-10-29
  • Contact: ZHANG Lan E-mail:lanizhg@126.com
  • Supported by:
    National Natural Science Foundation of China(81874351);National Natural Science Foundation of China(81703729);Beijing High-level Health and Technical Personal Plan(2014-2-014)

Abstract:

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases, which is characterized by cognitive and memory dysfunction. Calpain is widely activated in cells. Disturbance of calpain is currently thought to a main cause of hyperphosphorylation and abnormal cleavage of tau protein in AD pathology. Calpain affects the activities of glycogen synthase kinase 3 and protein phosphatase 2A, which causes abnormal hyperphosphorylation of multiple sites of tau protein, and mediates truncation of tau protein monomers, and induces neurodegeneration. Calpain is expected to be a potential target for drug therapy of AD.

Key words: calpain, Alzheimer's disease, tau protein, hyperphosphorylation, cleavage, review

CLC Number: