Please use this identifier to cite or link to this item: http://dora.health.qld.gov.au/qldresearchjspui/handle/1/1595
Title: Celecoxib in a Preclinical Model of Repetitive Mild Traumatic Brain Injury: Hippocampal Learning Deficits Persist with Inflammatory and Excitotoxic Neuroprotection
Authors: Matthew Hiskens 
Vella R
Schneiders A
Fenning A
Issue Date: 2021
Publisher: MDPI
Source: Hiskens, M., Vella, R., Schneiders, A., and Fenning, A. (2021) Celecoxib in a preclinical model of repetitive mild traumatic brain injury: hippocampal learning deficits persist with inflammatory and excitotoxic neuroprotection
Abstract: Repetitive mild traumatic brain injuries (mTBIs) contribute to inflammation-induced neurodegeneration. Cycloxygenase (COX) enzymes produce inflammatory cytokines that influence the microglia response to neurotrauma. Celecoxib is a selective COX-2 inhibitor that is prescribed in some conditions of mTBI to alleviate symptoms of concussion, and has shown benefits in neurodegenerative conditions. We investigated molecular pathways of neuroinflammation in response to celecoxib treatment in a mouse model of repetetive mTBI. Fifteen mTBIs were delivered over 23 days in adult male C57BL/6J mice in one of four groups (control, celecoxib without impact, celecoxib with impact, and vehicle with impact). Cognitive function was assessed at 48 h and three months following the final mTBI. Morris Water Maze testing revealed impaired hippocampal spatial learning performance in the celecoxib treatment with the impact group compared to the vehicle with impact control in the acute phase, with celecoxib treatment providing no improvement compared with the control at chronic testing; mRNA analysis of the cerebral cortex and hippocampus revealed expression change, indicating significant improvement in microglial activation, inflammation, excitotoxicity, and neurodegeneration at chronic measurement. These data suggest that, in the acute phase following injury, celecoxib protected against neuroinflammation, but exacerbated clinical cognitive disturbance. Moreover, while there was evidence of neuroprotective alleviation of mTBI pathophysiology at chronic measurement, there remained no change in clinical features.
Description: The funding source was not involved in any of the following: study design; collection, analysis, and interpretation of data; writing of the report; or decision to submit the article for publication.
DOI: 10.3390/traumacare1010003
Keywords: Mild Traumatic Brain Injury;Hippocampal Learning Deficits;Animal Studies;Celecoxib;Inflammatory and Excitotoxic Neuroprotection
Type: Article
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