Various types of brain injuries including traumatic brain injury (TBI), transiently but robustly increase neurogenesis while the neuroinflammatory response to injury takes place. Paradoxically, TBI subsequently causes long-term deficits in neurogenesis. This may be due to stem cell exhaustion. TBI is recognized as an important risk factor for neurodegenerative diseases, as persistent and prolonged neuroinflammation following a traumatic event has been linked to neurodegeneration.
Addressing TBI, within the realm of rodent and human investigations, neuroinflammatory, neurodegenerative, and neuroregenerative mechanisms post-trauma, it is important to emphasize the current substantial contribution of domestic violence to TBI rates and different types of injury, including concussion and mild TBI (direct injury to the head and/or strangulation) particularly affecting women.
While a few studies suggest little or no sex differences in post-traumatic neurogenesis, one critical issue is the assumption that post-TBI changes in neurogenesis similarly affect cognitive recovery in males and females in a similar way.
Human studies report poorer long-term outcomes for women compared to men after TBI.
Unfortunately, the impact of TBI on neurological and cognitive recovery mechanisms in female subjects remains significantly understudied.
Moreover, it is unknown whether sex differences exist in the long-term effects of TBI on constitutive neurogenesis or whether impairments in neurological recovery mechanisms pose a sex-dependent risk for age or disease-related cognitive decline.
On the other hand, discrepancies between outcomes from rodent models and human studies should be noted, as evidence of the compensatory mechanisms of females following TBI has been reported in rodents.
Overall, we need a clearer understanding of endogenous mechanisms of recovery following TBI, bridging the knowledge gap between rodent models and human reports, and emphasizing sex differences.
This Research Topic aims to dissect the cascade of events post-TBI, altering the trajectory of healthy brain aging. It focuses on sex differences in the neuroinflammatory response, and neurodegenerative and regenerative processes, which mainly influence endogenous recovery mechanisms, aging, and disease risk, and which could inform and help develop novel potential pharmacological interventions.
We welcome articles addressing:
● Sex differences in neurodegeneration and regeneration after injury, inflammation, cell senescence, cell death, growth factors, axonal regeneration, neurogenesis, and angiogenesis in the context of functional recovery
● Evidence of the compensatory mechanism of females following TBI in rodents
● Preconditioning and adaptive processes
● Pharmacological insights in targeting neuroinflammation post-trauma
● Incidence of Alzheimer’s disease (AD) and progressive diseases in female subjects with a history of TBI
● Neuroprotective effects of hormones on impacted females
● TBI outcomes: Ischemia, stroke, seizures as a long-term result of TBI insult
● Neurogenesis and genetic changes
● Neurovascular and metabolic dysregulation following TBI
● Endogenous recovery factors
● Cognitive outcomes following TBI and recovery targeting neuroinflammation shortly after the lesion
Within a broader context, research articles should try to spotlight the contribution of domestic violence to TBI, collecting studies to enhance awareness of domestic violence-triggered TBI.
Keywords:
neurogenesis, TBI, concussive injury, sub-concussive injury, domestic violence, sex differences, regeneration, degeneration, neuroinflammation, cognitive deterioration, anti-inflammatory agents, female rodent models
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.
Various types of brain injuries including traumatic brain injury (TBI), transiently but robustly increase neurogenesis while the neuroinflammatory response to injury takes place. Paradoxically, TBI subsequently causes long-term deficits in neurogenesis. This may be due to stem cell exhaustion. TBI is recognized as an important risk factor for neurodegenerative diseases, as persistent and prolonged neuroinflammation following a traumatic event has been linked to neurodegeneration.
Addressing TBI, within the realm of rodent and human investigations, neuroinflammatory, neurodegenerative, and neuroregenerative mechanisms post-trauma, it is important to emphasize the current substantial contribution of domestic violence to TBI rates and different types of injury, including concussion and mild TBI (direct injury to the head and/or strangulation) particularly affecting women.
While a few studies suggest little or no sex differences in post-traumatic neurogenesis, one critical issue is the assumption that post-TBI changes in neurogenesis similarly affect cognitive recovery in males and females in a similar way.
Human studies report poorer long-term outcomes for women compared to men after TBI.
Unfortunately, the impact of TBI on neurological and cognitive recovery mechanisms in female subjects remains significantly understudied.
Moreover, it is unknown whether sex differences exist in the long-term effects of TBI on constitutive neurogenesis or whether impairments in neurological recovery mechanisms pose a sex-dependent risk for age or disease-related cognitive decline.
On the other hand, discrepancies between outcomes from rodent models and human studies should be noted, as evidence of the compensatory mechanisms of females following TBI has been reported in rodents.
Overall, we need a clearer understanding of endogenous mechanisms of recovery following TBI, bridging the knowledge gap between rodent models and human reports, and emphasizing sex differences.
This Research Topic aims to dissect the cascade of events post-TBI, altering the trajectory of healthy brain aging. It focuses on sex differences in the neuroinflammatory response, and neurodegenerative and regenerative processes, which mainly influence endogenous recovery mechanisms, aging, and disease risk, and which could inform and help develop novel potential pharmacological interventions.
We welcome articles addressing:
● Sex differences in neurodegeneration and regeneration after injury, inflammation, cell senescence, cell death, growth factors, axonal regeneration, neurogenesis, and angiogenesis in the context of functional recovery
● Evidence of the compensatory mechanism of females following TBI in rodents
● Preconditioning and adaptive processes
● Pharmacological insights in targeting neuroinflammation post-trauma
● Incidence of Alzheimer’s disease (AD) and progressive diseases in female subjects with a history of TBI
● Neuroprotective effects of hormones on impacted females
● TBI outcomes: Ischemia, stroke, seizures as a long-term result of TBI insult
● Neurogenesis and genetic changes
● Neurovascular and metabolic dysregulation following TBI
● Endogenous recovery factors
● Cognitive outcomes following TBI and recovery targeting neuroinflammation shortly after the lesion
Within a broader context, research articles should try to spotlight the contribution of domestic violence to TBI, collecting studies to enhance awareness of domestic violence-triggered TBI.
Keywords:
neurogenesis, TBI, concussive injury, sub-concussive injury, domestic violence, sex differences, regeneration, degeneration, neuroinflammation, cognitive deterioration, anti-inflammatory agents, female rodent models
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.