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Celecoxib in a Preclinical Model of Repetitive Mild Traumatic Brain Injury: Hippocampal Learning Deficits Persist with Inflammatory and Excitotoxic Neuroprotection 塞来昔布在重复性轻度外伤性脑损伤的临床前模型:海马体学习缺陷持续存在炎症和兴奋毒性神经保护

Trauma care (Basel, Switzerland) Pub Date : 2021-03-26 DOI: 10.3390/TRAUMACARE1010003

Matthew I. Hiskens, R. Vella, A. Schneiders, A. Fenning

{"title":"Celecoxib in a Preclinical Model of Repetitive Mild Traumatic Brain Injury: Hippocampal Learning Deficits Persist with Inflammatory and Excitotoxic Neuroprotection","authors":"Matthew I. Hiskens, R. Vella, A. Schneiders, A. Fenning","doi":"10.3390/TRAUMACARE1010003","DOIUrl":"https://doi.org/10.3390/TRAUMACARE1010003","url":null,"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.","PeriodicalId":75251,"journal":{"name":"Trauma care (Basel, Switzerland)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/TRAUMACARE1010003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41984225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Effects of Memantine in Patients with Traumatic Brain Injury: A Systematic Review 美金刚在外伤性脑损伤患者中的作用:一项系统综述

Trauma care (Basel, Switzerland) Pub Date : 2021-01-27 DOI: 10.3390/TRAUMAS1010001

Sungeen Khan, Ayesha S Ali, B. Kadir, Z. Ahmed, V. Di Pietro

{"title":"Effects of Memantine in Patients with Traumatic Brain Injury: A Systematic Review","authors":"Sungeen Khan, Ayesha S Ali, B. Kadir, Z. Ahmed, V. Di Pietro","doi":"10.3390/TRAUMAS1010001","DOIUrl":"https://doi.org/10.3390/TRAUMAS1010001","url":null,"abstract":"Traumatic brain injury (TBI) affects millions of people around the world and amongst other effects, causes cognitive decline, neurodegenerative disease and increased risk of seizures and sensory disturbances. Excitotoxicity and apoptosis occur after TBI and are mediated through the N-methyl-D-aspartate (NMDA)-type glutamate receptor. Memantine is effective in blocking excessive activity of NMDA-type glutamate receptors and reduces the progression of dementia and may have benefits after TBI. Here, we performed a systematic review of the literature to evaluate whether memantine is effective in improving outcomes, including cognitive function in patients with TBI. Our search yielded only 4 randomized control trials (RCTs) that compared the effects of memantine to placebos, standard treatment protocols or piracetam. A single RCT reported that serum neuron-specific enolase (NSE) levels were significantly reduced (p = 0.009) in the memantine compared to the control group, and this coincided with reported significant day-to-day improvements in Glasgow Coma Scale (GCS) for patients receiving memantine. The remaining RCTs investigated the effects of memantine on cognitive function using 26 standardized tests for assessing cognition function. One RCT reported significant improvements in cognitive function across all domains whilst the other two RCTs, reported that patients in the memantine group underperformed in all cognitive outcome measures. This review shows that despite laboratory and clinical evidence reporting reduced serum NSE and improved GCS, supporting the existence of the neuroprotective properties, there is a lack of reported evidence from RCTs to suggest that memantine directly leads to cognitive improvements in TBI patients.","PeriodicalId":75251,"journal":{"name":"Trauma care (Basel, Switzerland)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/TRAUMAS1010001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47423588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

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