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

• Type of Material: Article
• Authors: Andrew Erwood, Emory University; Ali M Alawieh, Emory University
• Language: English
• Date: 2022-02-28
• Publisher: Medknow Publications
• Publication Version: Final Published Version
• Copyright Statement: © Neural Regeneration Research
• License: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.4103/1673-5374.335799
• Title of Journal or Parent Work: Neural Regeneration Research
• Volume: 17
• Issue: 10
• Start Page: 2228
• End Page: 2229
• Keywords: brain injury; inflammatory disease
• Research Categories: Health Sciences, Medicine and Surgery

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).