| Literature DB >> 32176646 |
Teodor T Postolache1,2,3,4, Abhishek Wadhawan1,5, Adem Can6, Christopher A Lowry2,3,7,8, Margaret Woodbury1,9, Hina Makkar1, Andrew J Hoisington2,10, Alison J Scott11, Eileen Potocki9, Michael E Benros12, John W Stiller1,13,14.
Abstract
There is an increasing evidence that inflammation contributes to clinical and functional outcomes in traumatic brain injury (TBI). Many successful target-engaging, lesion-reducing, symptom-alleviating, and function-improving interventions in animal models of TBI have failed to show efficacy in clinical trials. Timing and immunological context are paramount for the direction, quality, and intensity of immune responses to TBI and the resulting neuroanatomical, clinical, and functional course. We present components of the immune system implicated in TBI, potential immune targets, and target-engaging interventions. The main objective of our article is to point toward modifiable molecular and cellular mechanisms that may modify the outcomes in TBI, and contribute to increasing the translational value of interventions that have been identified in animal models of TBI.Entities:
Keywords: Depression; glia; immune challenge; immunomodulation; inflammation; priming; probiotic; traumatic brain injury
Mesh:
Year: 2020 PMID: 32176646 PMCID: PMC8190673 DOI: 10.3233/JAD-191150
Source DB: PubMed Journal: J Alzheimers Dis ISSN: 1387-2877 Impact factor: 4.472