中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (10): 2228-2229.doi: 10.4103/1673-5374.335799

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

补体激活引发急性创伤后脑损伤向慢性炎症性疾病的转变

  

  • 出版日期:2022-10-15 发布日期:2022-03-16

Complement activation kindles the transition of acute post-traumatic brain injury to a chronic inflammatory disease

Andrew Erwood, Ali M. Alawieh   

  1. Department of Neurosurgery, Emory University School of Medicine, Atlanta, GA, USA
  • Online:2022-10-15 Published:2022-03-16
  • Contact: Ali M. Alawieh, MD, PhD, ali.mostafa.alawieh@emory.edu.

摘要: https://orcid.org/0000-0003-2601-8850 (Ali M. Alawieh)

Abstract: Traumatic brain injury (TBI) remains a major cause of disability among young adults in both civilian and military settings contributing to a high burden on healthcare systems (Badhiwala et al., 2019). Sequel of TBI, even mild injuries, include motor and sensory dysfunction, neurocognitive decline, neuropsychiatric complications, as well as increased risk of neurodegenerative and neurovascular events such as Alzheimer’s disease and stroke (Breunig et al., 2013; Burke et al., 2013; Li et al., 2017). Despite the acute nature of the insult in TBI, pathological changes in the traumatized brain are better recognized as a chronic rather than an acute neurological disease, a phenomenon that remains under-investigated. Robust clinical data support the role of neuroinflammation in propagating neurodegenerative changes following TBI with a pivotal role of the complement system as an early trigger and chronic propagator of this response (Alawieh et al., 2018, 2021; Mallah et al., 2021). Hereby, we discuss how the role of complement pathways in different phases of injury after TBI was investigated using clinically relevant targeted complement inhibitors (Alawieh and Tomlinson, 2016; Alawieh et al., 2018, 2021; Mallah et al., 2021).