Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury

The neuroinflammatory hypothesis of traumatic brain injury (TBI) broadly states that neuroinflammatory mechanisms underlie many of the negative sequela of TBI. Each year, millions of people experience a TBI, with worldwide estimates suggesting as many as 69 million people suffer a TBI annually. In the United States alone, more than 40 million Americans over 40 years of age are living with TBI. Suffering a TBI increases the 30-year mortality rate by 2.2 – 2.9x, and it frequently induces depression, cognitive impairment, and other neurobehavioral dysfunction. TBI also increases susceptibility to acute and chronic neurodegenerative disorders, including epilepsy, Parkinson’s disease, and Alzheimer’s disease. Although clinical trials for TBI biomarkers and therapeutics have largely failed, major advances in the identification of functional neuroimmune and neuroinflammatory mechanisms hold renewed promise as important post-traumatic therapeutic targets. This Collection seeks to explore these novel functional mechanisms after TBI with an eye towards elucidating and modifying the pathogenic progression to the various post-traumatic syndromes.

As part of this Collection, we invite articles that include:

• Innate immune and neuroimmune mechanisms, including DAMP’s and complement signaling
• Adaptive immune and neuroimmune mechanisms
• Meningeal lymphatics, glymphatic, lymphatic dysfunction in TBI
• Gut/neuroinflammatory axis
• Vascular/neuroimmune axis
• Immune cell/brain cell interactions
• Immunometabolism and TBI
• Neuroinflammatory biomarkers of TBI severity and outcomes
• Sex as a biological variable in the neuroimmune response to injury
• Translational human immune mechanisms
• Astrocyte and microglial mechanisms and function