Let’s continue the topic “Epilepsy”. It is reported that REST will be strongly induced in hippocampal pyramidal and dentate granule neurons after pilocarpine-induced status epilepticus (SE), indicating that REST may be an excellent candidate transcription factor to mediate seizure-induced widespread changes in gene expression.
Recently, more direct evidence shows that REST knockout mice exhibits dramatically accelerated seizure progression and prolonged after discharge duration. Thus, REST may produce a negative effect on epileptogenesis. Further studies suggest that both REST expression and target protein HDAC activity seem critical for ischemia-induced neurodegeneration. For example, the antiepileptic valproic acid (VPA) block seizure-induced aberrant neurogenesis by inhibiting HDAC activity and normalizing REST-regulated gene expression, and thus protects epileptic rats from hippocampus-dependent cognitive impairment after induced seizures.
Besides, disruptions of gene programs regulated by other transcriptional factors, such as MeCP2 and CREB, are also found to be related to the pathology of RTT syndrome and epilepsy.
At present, seizure-preventing drugs or anti-epileptic drugs will be used in the treatment of Epilepsy. Sometimes surgery may stop them. Some anti-epileptic drugs are effective with a limited number of types of seizure, while others may treat a broader range. However, the best way is to find the disease as soon as possible, and try to avoid its development.