Neuroinflammation and neurodegeneration following traumatic brain injuries

Abstract

Traumatic brain injuries (TBI) commonly occur following head trauma. TBI may result in short- and long-term complications which may lead to neurodegenerative consequences, including cognitive impairment post-TBI. When investigating the neurodegeneration following TBI, studies have highlighted the role reactive astrocytes have in the neuroinflammation and degeneration process. This review showcases a variety of markers that show reactive astrocyte presence under pathological conditions, including glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3 (C3) and S100A10. Astrocyte activation may lead to white-matter inflammation, expressed as white-matter hyperintensities. Other white-matter changes in the brain following TBI include increased cortical thickness in the white matter. This review addresses the gaps in the literature regarding post-mortem human studies focussing on reactive astrocytes, alongside the potential uses of these proteins as markers in the future studies that investigate the proportions of astrocytes in the post-TBI brain has been discussed. This research may benefit future studies that focus on the role reactive astrocytes play in the post-TBI brain and may assist clinicians in managing patients who have suffered TBI.

Keywords: Neurodegeneration; Neuroinflammation; Reactive astrocytes; Traumatic brain injury.

Fig. 1

Effect of time on cortical thickness in TBI group. Coloured areas represent the location of vertices that demonstrate a significant change in cortical thickness over time (10% false discovery rate [FDR] corrected), where darker shades reflect the most substantial changes (see colour bar). Cortical thickness at single vertices indicated by crosshairs on the cortical surfaces above are plotted to illustrate cortical thickness changes over time. a Regions of the cortex decrease in thickness over time. b Regions of the cortex increase in thickness over time (Mazaharally et al. 2022)

Fig. 2

The blue represents regions of reduced resting-stated functional connectivity in the patients with high frontal WMH volume (Patient-A) compared with patients with low frontal WMH volume (Patient-B) and the control. Cluster extent threshold of P value of 0.01 using an Family-Wise Error (FWE) correction for multiple comparisons (Zhang et al. 2022)