Epigenetics in epilepsy.

作者: K. Kobow , I. Blümcke

DOI: 10.1016/J.NEULET.2017.01.012

关键词:

摘要: Approximately 50 million people have epilepsy, making it the most common chronic and severe neurological disease worldwide, with increased risk of mortality psychological socioeconomic consequences impairing quality life. More than 30% patients epilepsy inadequate control their seizures drug therapy. Any structural brain lesion can provoke epilepsy. However, progression seizure activity as well development drug-resistance remains difficult to predict, irrespective underlying epileptogenic condition, i.e., traumatic injury, developmental lesions, tumors or genetic inheritance. Mutated DNA sequences in genes encoding for ion channels neurotransmitter receptors been identified hereditary focal generalized epilepsies, but genotype-phenotype correlations are poor, arguing additional factors determining effect a predisposition. The dynamics epigenetic mechanisms (e.g. methylation, histone modifications, chromatin remodelling, non-coding RNAs) provide likely explanations features other complex diseases, including late onset, parent-of-origin effects, discordance monozygotic twins, fluctuation symptoms. In addition, many cortical dysplasias (FCDs), glio-neuronal ganglioglioma), temporal lobe hippocampal sclerosis (TLE-HS), do not seem primarily associate traits, suggesting pathogenic mechanisms. Herein we will discuss faces machinery, which provides powerful tools propagate epileptogenicity also contribute memory difficult-to-treat epilepsies.

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