New progress of mitochondrial dysfunction in the pathogenesis of Parkinson′s disease
10.3760/cma.j.cn431274-20200608-00760
- VernacularTitle:线粒体功能障碍在帕金森病发病机制研究中的新进展
- Author:
Jie LIN
1
;
Tao CHEN
;
Jiali SU
;
Benchi CAI
;
Yanhui LIU
;
Danting ZENG
;
Qiang YANG
Author Information
1. 海南省人民医院神经内科，海口 570311
- Keywords:
Parkinson disease;
Mitochondria;
Alpha-synuclein
- From:
Journal of Chinese Physician
2021;23(8):1269-1274
- CountryChina
- Language:Chinese
-
Abstract:
Parkinson′s disease (PD) is a neurodegenerative disease commonly found in middle-aged and elderly people. It is characterized by resting tremor, bradykinesia, myotonia, and abnormal posture gait. The main pathological changes were the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy bodies in the cytoplasm of the residual neurons. The main component of the Lewy bodies was α-synuclein. And why it causes the degeneration of dopaminergic neurons in the substantia nigra is not known. At present, most studies on Parkinson′s disease focus on the pathogenesis of the disease. More and more evidence shows that respiratory chain injury is a key feature of sporadic PD patients, and the proteins encoded by PD-related genes are related to the disorder of mitochondrial function. We believe that the important mechanism of the disease is impaired mitochondrial function due to environmental and (or) genetic inheritance. This article highlights new advances in mitochondrial dysfunction in Parkinson′s pathogenesis, including mitochondria and cell-mediated immunity, endoplasmic reticulum (ER)-mitochondrial axis, sirtuin-mediated mitochondrial stress response, and the role of microRNA in the etiology of PD. A deeper understanding of these mechanisms may provide inspiration for the development of new targeted therapies.
