中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (9): 4257-4258.doi: 10.4103/NRR.NRR-D-25-01192

• 观点:退行性病与再生 • 上一篇    下一篇

α-突触核蛋白结构变异驱动 Tau 病理学和疾病的互作

  

  • 出版日期:2026-09-15 发布日期:2026-05-14

Alpha-synuclein structural variantsdriving tau pathology and disease interaction

Chuanqi Sun*   

  1. Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA, USA
    Departments of Biological Chemistry and Chemistry and Biochemistry, UCLA-DOE Institute, UCLA, CA, USA

  • Online:2026-09-15 Published:2026-05-14
  • Contact: Chuanqi Sun, PhD, sunchuanqi@g.ucla.edu.

摘要: https://orcid.org/0000-0002-6443-6407 (Chuanqi Sun)

Abstract: Redefining neurodegenerative diseases: from isolated protein pathologies to intertwined disease networks: A common feature of neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Lewy body dementia, and multiple system atrophy is the accumulation of misfolded, insoluble protein aggregates in specific neurons or glial cells. In AD, these aggregates are mainly manifested as neurofibrillary tangles composed of Tau protein, while in PD, they are mainly manifested as Lewy bodies composed of α-synuclein.