A neuroinflammatory response is a universal feature of traumatic brain injury (TBI), highly involved in the initiation, development, and deterioration/recovery of TBI. We have long been aware of the dual roles that neuroinflammation plays in the pathogenesis of TBI, that different neuroimmune factors have both neurotoxic and neuroprotective effects after TBI. While there are some controversial findings concerning the benefits or detrimental roles of acute neuroinflammation, it is generally believed that chronic neuroinflammation is a key contributor to the persistent and progressive neurodegeneration often observed following TBI, and is associated with posttraumatic epilepsy, sleeping disorders, chronic pain, depression, dementia, and motor abnormalities.
There are a few key components of the acute or prolonged neuroinflammatory response, namely glial cells (microglia and astrocytes), circulating leukocytes (neutrophils, monocytes, and lymphocytes), and a vast array of bioactive cytokines. The exact neurotoxic or neuroprotective role that each of these factors exerts at different stages of TBI remains unclear. We are also not very clear about the circumstances under which these factors are detrimental or beneficial – e.g. does age or sex matter? Despite the fact that a large majority of TBI patients are children, elderly, and female, the majority of TBI research to date has been performed in adult-males, and our understanding of the neuroinflammatory response to TBI in these particular settings is very limited.
We call for thoughts and findings to collectively provide insights into these questions and discuss the beneficial and/or detrimental effects of neuroinflammation on TBI outcomes. We welcome both animal and human studies, and all kinds of article types.
A neuroinflammatory response is a universal feature of traumatic brain injury (TBI), highly involved in the initiation, development, and deterioration/recovery of TBI. We have long been aware of the dual roles that neuroinflammation plays in the pathogenesis of TBI, that different neuroimmune factors have both neurotoxic and neuroprotective effects after TBI. While there are some controversial findings concerning the benefits or detrimental roles of acute neuroinflammation, it is generally believed that chronic neuroinflammation is a key contributor to the persistent and progressive neurodegeneration often observed following TBI, and is associated with posttraumatic epilepsy, sleeping disorders, chronic pain, depression, dementia, and motor abnormalities.
There are a few key components of the acute or prolonged neuroinflammatory response, namely glial cells (microglia and astrocytes), circulating leukocytes (neutrophils, monocytes, and lymphocytes), and a vast array of bioactive cytokines. The exact neurotoxic or neuroprotective role that each of these factors exerts at different stages of TBI remains unclear. We are also not very clear about the circumstances under which these factors are detrimental or beneficial – e.g. does age or sex matter? Despite the fact that a large majority of TBI patients are children, elderly, and female, the majority of TBI research to date has been performed in adult-males, and our understanding of the neuroinflammatory response to TBI in these particular settings is very limited.
We call for thoughts and findings to collectively provide insights into these questions and discuss the beneficial and/or detrimental effects of neuroinflammation on TBI outcomes. We welcome both animal and human studies, and all kinds of article types.
