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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

The protective mechanism of SIRT3 and potential therapy in acute kidney injury

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