中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (8): 1723-1724.doi: 10.4103/1673-5374.363831

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

神经退行性疾病中伴侣介导的自噬:分子机制和药理学机会

  

  1. 中药质量研究国家重点实验室,中华医学研究院,澳门大学,中国
  • 出版日期:2023-08-15 发布日期:2023-02-23

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.

摘要: https://orcid.org/0000-0002-1147-125X (Jia-Hong Lu) 

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).