Life and death in the hippocampus: What's bad?

Protective effects of chlorogenic acid on trimethyltin chloride-induced neurobehavioral dysfunctions in mice relying on the gut microbiota

“…Hippocampal neuronal degeneration occurs in various neurodegenerative disorders and is deeply associated with neurobehavior abnormalities such as cognitive impairment and epilepsy-like seizure. 8,9 The c-Jun N-terminal kinase (JNK; also referred to as the stress-activated protein kinase) pathway appears to be one particular crucial apoptotic pathway in neurons. 10 JNKs are phosphorylated and activated in neurons in response to various stimuli, wherein c-Jun, a well-defined downstream target of JNK, plays an obligatory role in the death process.…”

Seizure-Induced Oxidative Stress in Status Epilepticus: Is Antioxidant Beneficial?

“…Status epilepticus has a 10–20% mortality in previous studies [ 13 , 17 ], although more rapid treatment regimens at an early stage reduce disease-related mortality in recent studies [ 12 , 19 ]. Human and animal studies also revealed that status epilepticus causes substantial cerebral damage, raises the risk to develop succeeding epileptic episodes, and accompanies with a distinctive pattern of neuronal death in the hippocampus, such as in dentate gyrus hilus, CA3, and CA1 subfield [ 20 , 21 ].…”

Exercise-linked consequences on epilepsy

“…The net sum of both processes might determine the course of the disease, through a mechanism that might address the brain-derived neurotrophic factor (BDNF) role [78]. The decrease in the neurogenesis and the increase in the number of neuronal deaths occurs mainly in the hippocampus, affect short-and long-term memory leading to cognitive decline in epilepsy [79]. Aerobic physical exercise [80] and resistance training [81] are capable of reversing the cognitive decline caused by epilepsy, inhibiting neuronal apoptosis in rodents [82].…”