中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (9): 1869-1870.doi: 10.4103/1673-5374.390979

• 观点:退行性病与再生 • 上一篇    下一篇

自身溶酶体酸化损伤作为TNFR1诱导阿尔茨海默病神经元坏死的介质

  

  • 出版日期:2024-09-15 发布日期:2024-01-25

Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer’s disease

Evridiki Asimakidou, Richard Reynolds, Anna M. Barron, Chih Hung Lo*   

  1. Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK (Asimakidou E)
    Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, UK (Reynolds R) 
    Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore (Barron AM, Lo CH)
  • Online:2024-09-15 Published:2024-01-25
  • Contact: Chih Hung Lo, PhD, chihhung.lo@ntu.edu.sg.
  • Supported by:
    This work was supported by a Lee Kong Chian School of Medicine Dean’s Postdoctoral Fellowship (021207-00001) from Nanyang Technological University Singapore and a Mistletoe Research Fellowship (022522-00001) from the Momental Foundation USA (to CHL).

摘要: https://orcid.org/0000-0003-2717-4484 (Chih Hung Lo)

Abstract: Neuronal necroptosis–an emerging form of regulated cell death associated with neuroinflammatory signaling: Alzheimer’s disease (AD) is characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles as well as progressive neuronal loss. Recent evidence has suggested that prolonged neuroinflammation with increased levels of cytokines, arising from neuronal injury, innate immune responses from glial cells, and peripheral inflammation, leads to neuronal death and AD progression. Neuronal necroptosis is an emerging form of regulated cell death associated with neuroinflammatory signaling. Necroptosis typically occurs in response to sustained inflammation while apoptosis facilitates normal turnover of cellular contents important for growth and development. By combining features of apoptosis and necrosis, necroptosis has been proposed to constitute a more comprehensive mechanistic explanation for neurodegeneration, which is less likely to occur by the immunologically silent apoptotic cell death or by the acute occurrence of necrosis after cellular stress (Jayaraman and Reynolds, 2022).