The neuroinflammatory hypothesis of traumatic brain injury (TBI) suggests that neuroinflammatory processes are critical contributors to the adverse outcomes following TBI. Each year, millions of individuals sustain a TBI, with global estimates indicating that up to 69 million people are affected annually. In the United States alone, over 40 million Americans aged 40 and above live with the long-term effects of TBI. Experiencing a TBI increases the 30-year mortality rate by 2.2% to 2.9% and often results in depression, cognitive impairment, and various other neurobehavioral issues. Additionally, TBI heightens the risk of developing both acute and chronic neurodegenerative disorders, such as epilepsy, Parkinson’s disease, and Alzheimer’s disease. Despite the largely unsuccessful clinical trials for TBI biomarkers and treatments, significant progress in identifying functional neuroimmune and neuroinflammatory mechanisms offers renewed hope for effective post-traumatic therapeutic interventions.
This Collection aims to delve deeply into the novel functional mechanisms that emerge following traumatic brain injury (TBI), with the goal of understanding and influencing the pathological progression that leads to various post-traumatic syndromes. By examining these mechanisms in detail, the Collection seeks to shed light on how they contribute to the onset and development of conditions such as depression, cognitive impairment, and neurodegenerative diseases. The ultimate objective is to identify potential therapeutic targets that can be used to intervene in these processes, thereby improving outcomes for individuals who have suffered a TBI. Through this comprehensive exploration, we hope to advance the field of neuroinflammation and neuroimmune research, paving the way for new treatments and interventions that can mitigate the long-term effects of TBI.
Scope and Information for authors:
1. Mechanisms of innate immune and neuroimmune responses
2. Adaptive immune and neuroimmune responses
3. Dysfunction in meningeal lymphatics, glymphatic system, and lymphatics in TBI
4. Gut-brain axis and neuroinflammatory processes
5. Vascular-neuroimmune interactions
6. Interactions between immune cells and brain cells
7. The role of immunometabolism in TBI
8. Neuroinflammatory biomarkers indicating TBI severity and outcomes
9. Human immune mechanisms and their translational potential
10. Functions and mechanisms of astrocytes and microglia
Keywords:
traumatic brain injury, neuroinflammation, immune cells, neurodegeneration, neurobehavioral impairment
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
The neuroinflammatory hypothesis of traumatic brain injury (TBI) suggests that neuroinflammatory processes are critical contributors to the adverse outcomes following TBI. Each year, millions of individuals sustain a TBI, with global estimates indicating that up to 69 million people are affected annually. In the United States alone, over 40 million Americans aged 40 and above live with the long-term effects of TBI. Experiencing a TBI increases the 30-year mortality rate by 2.2% to 2.9% and often results in depression, cognitive impairment, and various other neurobehavioral issues. Additionally, TBI heightens the risk of developing both acute and chronic neurodegenerative disorders, such as epilepsy, Parkinson’s disease, and Alzheimer’s disease. Despite the largely unsuccessful clinical trials for TBI biomarkers and treatments, significant progress in identifying functional neuroimmune and neuroinflammatory mechanisms offers renewed hope for effective post-traumatic therapeutic interventions.
This Collection aims to delve deeply into the novel functional mechanisms that emerge following traumatic brain injury (TBI), with the goal of understanding and influencing the pathological progression that leads to various post-traumatic syndromes. By examining these mechanisms in detail, the Collection seeks to shed light on how they contribute to the onset and development of conditions such as depression, cognitive impairment, and neurodegenerative diseases. The ultimate objective is to identify potential therapeutic targets that can be used to intervene in these processes, thereby improving outcomes for individuals who have suffered a TBI. Through this comprehensive exploration, we hope to advance the field of neuroinflammation and neuroimmune research, paving the way for new treatments and interventions that can mitigate the long-term effects of TBI.
Scope and Information for authors:
1. Mechanisms of innate immune and neuroimmune responses
2. Adaptive immune and neuroimmune responses
3. Dysfunction in meningeal lymphatics, glymphatic system, and lymphatics in TBI
4. Gut-brain axis and neuroinflammatory processes
5. Vascular-neuroimmune interactions
6. Interactions between immune cells and brain cells
7. The role of immunometabolism in TBI
8. Neuroinflammatory biomarkers indicating TBI severity and outcomes
9. Human immune mechanisms and their translational potential
10. Functions and mechanisms of astrocytes and microglia
Keywords:
traumatic brain injury, neuroinflammation, immune cells, neurodegeneration, neurobehavioral impairment
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.