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ALC administration has been shown to decrease TNF activation in an epilepsy model ( We sought further evidence of the neuroinflammatory response to rmTBI and ALC treatment by examining the expression of CCL11, a chemokine that has received increased attention in TBI ( Another important secondary injury mechanism following mTBI is excitotoxicity, involving impaired neuronal calcium regulation and glutamate release resulting in dendrite damage ( We further investigated whether the neuroprotective effects of ALC at the molecular level would translate into mitigation of behavioral and cognitive dysfunction seen following rmTBI