Neuroinflammation in the Evolution of Secondary Injury, Repair, and Chronic Neurodegeneration after Traumatic Brain Injury
By Dennis W. Simon, M. McGeachy, H. Bayır, R. Clark, David J. Loane, P. Kochanek. Nature Reviews Neurology, 2017
994 citations recorded by the source corpus.
The 'silent epidemic' of traumatic brain injury (TBI) has been placed in the spotlight as a result of clinical investigations and popular press coverage of athletes and veterans with single or repetitive head injuries. Neuroinflammation can cause acute secondary injury after TBI, and has been linked to chronic neurodegenerative diseases; however, anti-inflammatory agents have failed to improve TBI outcomes in clinical trials. In this Review, we therefore propose a new framework of targeted immunomodulation after TBI for future exploration. Our framework incorporates factors such as the time from injury, mechanism of injury, and secondary insults in considering potential treatment options. Structuring our discussion around the dynamics of the immune response to TBI — from initial triggers to chronic neuroinflammation — we consider the ability of soluble and cellular inflammatory mediators to promote repair and regeneration versus secondary injury and neurodegeneration. We summarize both animal model and human studies, with clinical data explicitly defined throughout this Review. Recent advances in neuroimmunology and TBI-responsive neuroinflammation are incorporated, including concepts of inflammasomes, mechanisms of microglial polarization, and glymphatic clearance. Moreover, we highlight findings that could offer novel therapeutic targets for translational and clinical research, assimilate evidence from other brain injury models, and identify outstanding questions in the field.
Subfields: Molecular Biology, Neurology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/5045e7fa814339a778997b90fd27ed47e0780227
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Citations in the corpus
- The IL-17 family of cytokines in health and disease (2019, background): “Also, traumatic or ischemic brain injury patients frequently develop dysbiosis during hospitalization, which could alter immune responses in the inflamed brain (Simon et al., 2017).”