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- W1590062562 abstract "Abstract : Long term effects of traumatic brain injury (TBI), including neuroendocrine dysregulation and neurobehavioral recovery may be ameliorated by intervention aimed at reducing short term neuroinflammation, oxidative stress, and altered neuroendocrine and behavioral functions. Our working hypothesis is that elevating levels of the endocannabinoids (EC), 2-arachidonoyl glycerol (2-AG) and N-arachidonoyl ethanolamine (AEA) should ameliorate neuroinflammatory changes following TBI. During this funding period, selective pharmacologic inhibitors have been used to decrease the degradation of 2-AG and/or AEA. Studies during this funding period are currently underway in an effort to prolong the duration of drug treatment to establish the optimal length of intervention. This is accomplished by administrating pharmacotherapy 30 min post-TBI, as well as an additional dose of the selective EC enzyme degradation inhibitors 24 hrs post TBI. Ongoing studies will continue to examine the extent to which this intervention has modulated cytokine release, neutrophil influx, blood brain barrier permeability, and neurological and neurobehavioral severity impairments following TBI." @default.
- W1590062562 created "2016-06-24" @default.
- W1590062562 creator A5030753158 @default.
- W1590062562 date "2012-11-01" @default.
- W1590062562 modified "2023-09-23" @default.
- W1590062562 title "Endocannabinoids as a Target for the Treatment of Traumatic Brain Injury" @default.
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- W1590062562 doi "https://doi.org/10.21236/ada576663" @default.
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