Pharmacologic Therapy for Traumatic Brain Injury
A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".
Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 6496
Special Issue Editor
Interests: neurons; ischemia; astrocytes; inflammatory; protease-activated receptors; thrombin; glutamate toxicity; cytokines; coagulation; activated protein C; intracellular calcium; apoptosis; necrosis
Special Issue Information
Dear Colleagues,
Traumatic brain injury (TBI) is an insult to the brain from an external force that causes temporary or permanent impairment in functional, psychosocial, or physical abilities. TBI—the "silent epidemic"—contributes to worldwide death and disability more than any other traumatic insult. According to the World Health Organization, TBI became the third leading cause of mortality amongst all age groups in the year 2020.
Common causes of TBI include motor vehicle accidents, falls, sports injuries, violence, and increasingly war zone injuries.
The nature of TBI sequela, whether psychiatric, cognitive, or behavioral, is poorly understood. Despite substantial and ongoing pre-clinical and clinical studies, there remain significant gaps in knowledge of TBI, and there is a paucity of therapies to limit the disabling consequences of TBI or to foster neuroregeneration. Likewise, the use of pharmacological interventions to improve the symptoms, function, and outcome of TBI is still under development.
However, there are a number of pharmacological agents that inspire optimism. When treating neurological deficits medically, the proper use of these agents for particular TBI clinical scenarios (the timing and nature of symptoms, whether agents are administered in the acute or chronic phase after TBI, etc.) is important.
TBIs are an active area of study for neuroscience researchers. Numerous world laboratories are investigating the molecular and clinical factors of TBIs; for example, scientists are still learning how TBI and dementia are linked on a molecular level.
A TBI can cause brain-cell death and tissue degeneration, potentially leading to many negative clinical symptoms for the patient. Therapeutic approaches may involve targeting the molecular pathways that control cell death using agents that prevent excitotoxicity or mitochondria dysfunctions.
While there is much promising work under way, there are significant opportunities to focus on areas such as mild TBI, the post-acute and chronic TBI periods, and on therapies targeting mechanisms of neurorepair and neuroregeneration. Thus, the challenges that combination therapy presents are only beginning to be addressed, and it is likely that polypharmacy will eventually be needed to achieve maximal recovery after TBI.
In this Special Issue, we focus on how new pharmacological approaches can prevent negative clinical symptoms and neurodegeneration for particular TBI clinical scenarios.
Prof. Dr. Liubov Gorbacheva
Guest Editor
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Keywords
- brain injuries
- traumatic
- therapeutics
- cognition
- consciousness
- drug
- motor recovery
- rehabilitation
- stroke
- psychostimulants
- antidepressants
- functional deficits
- mitochondrial dysfunction
- excitotoxicity
- dementia
- neurorepair
- neurodegeneration
