中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3549-3550.doi: 10.4103/NRR.NRR-D-25-00681

• 观点:退行性病与再生 • 上一篇    下一篇

多系统萎缩症认知功能障碍的病因及治疗

  

  • 出版日期:2026-08-18 发布日期:2026-04-25

Etiology and therapeutics for cognitive dysfunction in multiple system atrophy

Yasuo Miki*, Koichi Wakabayashi   

  1. Department of Neuropathology, Biomedical Research Center, Hirosaki University Graduate School of Medicine, Hirosaki, Japan
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Yasuo Miki, MD, PhD, yasuomiki@hotmail.com.
  • Supported by:
    This work was supported by Hirosaki University Priority Research Grant for Future Innovation (to YM), JSPS KAKENHI Grant Numbers 24K10654 (to YM) and 23K24209 (to KW), and the Collaborative Research Project of the Brain Research Institute, Niigata University (to YM).

摘要: https://orcid.org/0000-0001-9375-9590 (Yasuo Miki)

Abstract: Neurodegenerative disease is characterized by the presence of inclusion bodies containing abnormal toxic proteins in the central nervous system. Physiological α-synuclein exists in the form of a monomer or dimer at the presynaptic nerve terminal. It serves as a key molecule to modulate endocytosis and exocytosis. However, under pathological conditions, α-synuclein adopts different conformations, being converted into toxic oligomers. The molecular weight of α-synuclein oligomers ranges from 25 to 180 kDa, and they do not form filamentous aggregates of α-synuclein. Subsequently, α-synuclein oligomers change to aggregates, including protofibrils and fibrils (Miki et al., 2022). This process has been implicated in the pathogenesis of neurodegenerative diseases collectively termed synucleinopathies, which include Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy (MSA).