Neural Regeneration Research ›› 2023, Vol. 18 ›› Issue (8): 1723-1724.doi: 10.4103/1673-5374.363831

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Targeting chaperone-mediated autophagy for Parkinson’s disease therapy

Yi-Ting Wang, Jia-Hong Lu*   

  1. State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao Special Administrative Region, China
  • Online:2023-08-15 Published:2023-02-23
  • Contact: Jia-Hong Lu, PhD, jiahonglu@um.edu.mo.
  • Supported by:
    This work was supported by the Science and Technology Development Fund, Macau SAR (No. 0128/2019/A3), Guangdong Basic and Applied Basic Research Foundation (No. 2022A1515012416), National Natural Science Foundation of China (No. 31871024), and the University of Macau grants (No. MYRG2019-00129-ICMS) awarded to JHL.

Abstract: Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease. Epidemiological projections for the global incidence of PD indicate that the number of people with PD might approach 12 million by 2040 (Adrissi and Fleisher, 2022). PD clinical symptoms include bradykinesia, resting tremors, rigidity, and non-motor symptoms such as depression, autonomic dysfunctions, sensory impairments, and sleep disruptions. The neuropathologies of PD are the continuous loss of dopaminergic neurons in the middle brain substantia nigra pars compacta and the accumulation of Lewy bodies which are mainly composed of fibrillar α-synuclein aggregates in neuronal somata. There is growing evidence showing that autophagy is a critical avenue for regulating PD pathogenesis. In 2004, mutant α-synuclein blocked chaperone-mediated autophagy (CMA) demonstrated the first connection between CMA malfunction and PD (Cuervo et al., 2004).