Excitotoxicity, neuroinflammation and oxidant stress as molecular bases of epileptogenesis and epilepsy-derived neurodegeneration: The role of vitamin E.

摘要: Glutamate-mediated excitotoxicity, neuroinflammation, and oxidative stress are common underlying events in neurodegeneration. This pathogenic "triad" characterizes the neurobiology of epilepsy, leading to seizure-induced cell death, increased susceptibility neuronal synchronization network alterations. Along with other maladaptive changes, these pave way spontaneous recurrent seizures progressive degeneration interested brain areas. In vivo models epilepsy available explore such epileptogenic mechanisms, also assessing efficacy chemoprevention therapy strategies at pre-clinical level. The kainic acid model pharmacological excitotoxicity epileptogenesis is one most investigated mimicking chronicization profile temporal lobe humans. Its cues include inflammatory death pathway activation, mitochondrial disturbances lipid peroxidation several regions brain, vulnerable being hippocampus. importance neuroinflammation as molecular damage was demonstrated this by possibility counteract related morphological functional changes organ vitamin E, main fat-soluble cellular antioxidant "conditional" co-factor enzymatic pathways involved polyunsaturated metabolism signaling. present review paper provides an overview literature supporting potential for a timely intervention E clinical management processes associated peroxidation, i.e. "triad".