Brain injury that occurs after birth is termed as “Acquired Brain injury (ABI)”. ABI is an umbrella term that refers to traumatic brain injury (TBI) and non-traumatic brain injury. TBI is an external blow (single or multiple) to the head. Its causes mostly include falls, motor vehicle accidents, sports-related injury, and violence. Non-Traumatic Brain Injury, on the other hand, is brain damage due to internal disease process, excluding congenital disorders, degenerative diseases, or brain trauma at birth.
Although the pathological mechanisms of secondary damage to the brain are still not fully understood, the consequential outcomes are very similar in different forms of ABI, suggesting a unifying mechanism. It includes neuroinflammation, vascular abnormalities, broad axonal injury, focal or disseminated atrophy, neuronal circuit disruption and cognitive dysfunction. Importantly, ABI accelerates brain-aging, suggesting involvement of mechanisms such as senescence, unfolded protein response (UPR), autophagy, circadian rhythms, and a shift in metabolism. However, there are still multiple gaps in our understanding of how these processes at cellular levels bring changes at tissue levels.
This Research Topic will bring together research that addresses the changes in cellular pathways and functioning during different forms of ABI. This topic also welcomes intervention studies focused on multimodal therapies aiming to improve clinical symptoms after ABI. Understanding the connection between ABI and different cellular responses will lay a strong foundation for future research to identify signalling molecules and molecular pathways as potential drug targets for therapies leading to a healthy ageing.
This Research Topic welcomes original research articles, clinical studies, reviews, mini reviews, and perspectives towards understanding the role of the ABI in brain-aging. The current Research Topic will include, but not be limited to, the following themes:
(1) Pre-clinical research in the association between Ageing, Neuroinflammation and dementia.
(2) Pre-clinical research in cellular senescence, UPR, autophagy, circadian rhythms and, metabolism in ABI and other neurodegenerative animal models.
(3) Clinical research in cognition evaluation, neuroimaging, dementia markers, analysis of early neurodegeneration.
Brain injury that occurs after birth is termed as “Acquired Brain injury (ABI)”. ABI is an umbrella term that refers to traumatic brain injury (TBI) and non-traumatic brain injury. TBI is an external blow (single or multiple) to the head. Its causes mostly include falls, motor vehicle accidents, sports-related injury, and violence. Non-Traumatic Brain Injury, on the other hand, is brain damage due to internal disease process, excluding congenital disorders, degenerative diseases, or brain trauma at birth.
Although the pathological mechanisms of secondary damage to the brain are still not fully understood, the consequential outcomes are very similar in different forms of ABI, suggesting a unifying mechanism. It includes neuroinflammation, vascular abnormalities, broad axonal injury, focal or disseminated atrophy, neuronal circuit disruption and cognitive dysfunction. Importantly, ABI accelerates brain-aging, suggesting involvement of mechanisms such as senescence, unfolded protein response (UPR), autophagy, circadian rhythms, and a shift in metabolism. However, there are still multiple gaps in our understanding of how these processes at cellular levels bring changes at tissue levels.
This Research Topic will bring together research that addresses the changes in cellular pathways and functioning during different forms of ABI. This topic also welcomes intervention studies focused on multimodal therapies aiming to improve clinical symptoms after ABI. Understanding the connection between ABI and different cellular responses will lay a strong foundation for future research to identify signalling molecules and molecular pathways as potential drug targets for therapies leading to a healthy ageing.
This Research Topic welcomes original research articles, clinical studies, reviews, mini reviews, and perspectives towards understanding the role of the ABI in brain-aging. The current Research Topic will include, but not be limited to, the following themes:
(1) Pre-clinical research in the association between Ageing, Neuroinflammation and dementia.
(2) Pre-clinical research in cellular senescence, UPR, autophagy, circadian rhythms and, metabolism in ABI and other neurodegenerative animal models.
(3) Clinical research in cognition evaluation, neuroimaging, dementia markers, analysis of early neurodegeneration.
