Journal
PHARMACEUTICS
Volume 14, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/pharmaceutics14010152
Keywords
excitotoxicity; traumatic brain injury; novel therapeutics; NMDA receptor; GABA; vitamin B12; astrocyte; calcium; oxidative stress; neuroinflammation
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Traumatic brain injury (TBI) is a major cause of increased morbidity and mortality, with consequences ranging from mild cognitive impairment to death. This review provides a comprehensive understanding of the various pathways involved in tissue damage following TBI. It summarizes the preclinical evidence of potential therapeutic interventions and describes the available clinical evaluation of novel drug targets.
Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality. Consequences vary from mild cognitive impairment to death and, no matter the severity of subsequent sequelae, it represents a high burden for affected patients and for the health care system. Brain trauma can cause neuronal death through mechanical forces that disrupt cell architecture, and other secondary consequences through mechanisms such as inflammation, oxidative stress, programmed cell death, and, most importantly, excitotoxicity. This review aims to provide a comprehensive understanding of the many classical and novel pathways implicated in tissue damage following TBI. We summarize the preclinical evidence of potential therapeutic interventions and describe the available clinical evaluation of novel drug targets such as vitamin B12 and ifenprodil, among others.
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