Traumatic Brain Injury: Mechanistic Insight on Pathophysiology and Potential Therapeutic Targets.
Komal ThapaHeena KhanThakur Gurjeet SinghAmarjot KaurPublished in: Journal of molecular neuroscience : MN (2021)
Traumatic brain injury (TBI) causes brain damage, which involves primary and secondary injury mechanisms. Primary injury causes local brain damage, while secondary damage begins with inflammatory activity followed by disruption of the blood-brain barrier (BBB), peripheral blood cells infiltration, brain edema, and the discharge of numerous immune mediators including chemotactic factors and interleukins. TBI alters molecular signaling, cell structures, and functions. Besides tissue damage such as axonal damage, contusions, and hemorrhage, TBI in general interrupts brain physiology including cognition, decision-making, memory, attention, and speech capability. Regardless of the deep understanding of the pathophysiology of TBI, the underlying mechanisms still need to be assessed with a desired therapeutic agent to control the consequences of TBI. The current review gives a brief outline of the pathophysiological mechanism of TBI and various biochemical pathways involved in brain injury, pharmacological treatment approaches, and novel targets for therapy.
Keyphrases
- traumatic brain injury
- brain injury
- oxidative stress
- white matter
- cerebral ischemia
- resting state
- severe traumatic brain injury
- peripheral blood
- subarachnoid hemorrhage
- induced apoptosis
- decision making
- functional connectivity
- working memory
- spinal cord injury
- blood brain barrier
- single cell
- multiple sclerosis
- mild traumatic brain injury
- cell therapy
- stem cells
- high resolution
- mass spectrometry
- endoplasmic reticulum stress
- mild cognitive impairment
- combination therapy
- replacement therapy
- pi k akt