JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE) ›› 2021, Vol. 41 ›› Issue (11): 1529-1534.doi: 10.3969/j.issn.1674-8115.2021.11.020

• Review • Previous Articles     Next Articles

Research progress of chaperone-mediated autophagy in Alzheimer's disease

Jun-hui CHEN1,2(), You-quan GU1(), Li-he YAO1, Wei ZHANG3, Huai-xiang WANG4   

  1. 1.Department of Neurology, The First Hospital of Lanzhou University, Lanzhou 730013, China
    2.The First School of Clinical Medicine of Lanzhou University, Lanzhou 730013, China
    3.Department of Stomatology, Lanzhou University Second Hospital, Lanzhou 730030, China
    4.Department of Intensive Care Unit, Ganzhou District People's Hospital of Zhangye City, Gansu Province, Zhangye 734000, China
  • Online:2021-11-28 Published:2021-12-03
  • Contact: You-quan GU;
  • Supported by:
    Natural Science Foundation of Gansu Province(20JR10RA671);Youth Science and Technology Foundation of Gansu Province(21JR1RA152)


Alzheimer's disease (AD) is a common neurodegenerative disease. Its main pathological change is senile plaque (SP) formed by massive accumulation of amyloid β-protein (Aβ) and neurofibrillary tangles (NFTs) formed by excessive phosphorylation and accumulation of Tau protein in cells. Chaperone-mediated autophagy (CMA) selectively transfers proteins with CMA motifs to lysosomes for degradation. When the autophagy process is impaired, Aβ and abnormal phosphorylated Tau protein will accumulate in neurons, which can destroy the normal function of cells and accelerate their death. Relevant studies have shown that CMA is an important pathway for abnormal protein degradation in early AD, and the inactivation of this pathway may play an important role in the progression of AD. This paper reviews the concept, and physiological role of CMA and the pathological relationship between CMA and AD, and elaborates the role of inactivation of CMA pathway in AD diseases, in order to provide new ideas for the research and treatment of AD pathogenesis.

Key words: chaperone-mediated autophagy (CMA), Alzheimer's disease (AD), Tau protein, amyloid β-protein (Aβ)

CLC Number: