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In addition, it results in the hyperactivation of the HPA axis, an increase in corticosterone levels, the impairment of hippocampal neurogenesis, the promotion of oxidative and nitrosative stress, the upregulation of markers of neuroinflammation, and the stimulation of neuronal apoptosis in cerebral cortex and hippocampus [206]

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Epidemiological and mechanistic studies indicate that neuropsychiatric sequelae are common across the full spectrum of TBI severity and may persist long after the acute injury phase [76]