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Dysfunction of neuronal metabolism is central to all forms of seizure activity. Clinical, genetic and metabolic studies have implicated mitochondria in the process. Alterations in electron transport, generation of reactive oxygen species, calcium metabolism and apoptosis all have been described in human and animal nervous tissue and reflect changes in mitochondrial physiology. Improved understanding of the molecular details underlying seizures has begun to provide rational approaches to the design of new treatment strategies.

Introduction to the mini-review series on mitochondrial matters in epilepsy