AI Article Synopsis
- Evidence shows that inflammation plays a significant role in the outcomes of traumatic brain injury (TBI) affecting both clinical and functional recovery.
- Many treatments that work well in animal studies do not translate effectively to human clinical trials due to factors like timing and the immune environment.
- The article aims to highlight immune system components involved in TBI and propose modifiable mechanisms that could enhance treatment outcomes and bridge the gap between animal research and human applications.
Article 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.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8190673 | PMC |
| http://dx.doi.org/10.3233/JAD-191150 | DOI Listing |
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