中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (6): 1197-1198.doi: 10.4103/1673-5374.385873

• 观点:退行性病与再生 • 上一篇    下一篇

衰老、线粒体功能障碍和炎症对帕金森病的影响

  

  • 出版日期:2024-06-15 发布日期:2023-11-17

Influence of aging, mitochondrial dysfunction, and inflammation on Parkinson’s disease

Davide Cossu*, Nobutaka Hattori   

  1. Department of Neurology, Juntendo University, Tokyo, Japan (Cossu D, Hattori N)
    Department of Biomedical Sciences, Sassari University, Sassari, Italy (Cossu D) 
  • Online:2024-06-15 Published:2023-11-17
  • Contact: Davide Cossu, PhD, davide@juntendo.ac.jp.
  • Supported by:
    This work was supported by JSPS KAKENHI (JP23K14675) and PRIN 2022 (202238WEHT) (to DC).

摘要: https://orcid.org/0000-0002-0557-9467 (Davide Cossu) 

Abstract: Aging is associated with chronic form of inflammation called inflammaging, which results from immune system changes. Inflammaging plays a crucial role in the pathogenesis of various neurodegenerative diseases (Dabravolski et al., 2022). Moreover, aging-related inflammation can be triggered by disrupted mitophagy, where the accumulation of molecular patterns associated with mitochondrial damage in the cytosol leads to the production of inflammatory cytokines and activation of the immune response. In our recent research, we investigated the impact of aging and mitochondrial dysfunction on neuroinflammation using a model of central nervous system (CNS) neuroinflammation in mice that lack genes associated with familial Parkinson’s disease (PD; Figure 1).