中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (5): 955-956.doi: 10.4103/1673-5374.385301

• 观点:退行性病与再生 • 上一篇    下一篇

TDP-43是加速创伤性脑损伤后阿尔茨海默病发展的关键分子

  

  • 出版日期:2024-05-15 发布日期:2023-10-31

TDP-43 is a key molecule accelerating development of Alzheimer’s disease following traumatic brain injury

Chu Chen*   

  1. Department of Cellular and Integrative Physiology, Long School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
  • Online:2024-05-15 Published:2023-10-31
  • Contact: Chu Chen, PhD, chenc7@uthscsa.edu or chen502@gmail.com.
  • Supported by:
    This work was supported by National Institutes of Health grants RF1NS076815 and R01AG058621.

摘要: https://orcid.org/0000-0003-1287-8059 (Chu Chen)

Abstract: Currently, more than 55 million people have dementia worldwide and Alzheimer’s disease (AD) is one of the most common causes of dementia in aging. However, no effective therapies are currently available for the prevention and treatment of AD. This is largely due to our limited understanding of the mechanisms underlying the neuropathogenesis of AD. It has widely been recognized that AD is heterogeneous and that multi-factors are contributing to the pathogenesis of AD. Accumulated evidence suggests that traumatic brain injury (TBI) is an important risk factor for the development of AD and dementia later in life (Guo et al., 2000; Johnson et al., 2010). However, the precise mechanism by which TBI contributes to developing AD has yet to be elucidated.