| Literature DB >> 33856647 |
Palvi Gotra1, Nidhi Bhardwaj1, Abhilash Ludhiadch1, Gagandeep Singh2, Anjana Munshi3.
Abstract
Epilepsy and migraine are both episodic disorders and share clinical as well as pathophysiological mechanisms. The prevalence of epilepsy in migraine patients is generally higher than normal as compared to general population and vice versa. Various environmental risk factors and genetic factors have been reported to be associated with susceptibility of these comorbid diseases. Specific genes have been implicated in the pathogenesis of the two diseases. However, the shared genetic susceptibility has not been explored extensively. Previous studies have reported that the alterations in the genes encoding ion channel proteins are common risk factors for both the diseases. The alterations in ion channel-encoding genes CACNAIA (T666M) and SCNIA (Q1489K and L1649Q) have been found to be involved in the development of familial hemiplegic migraine (FHM) as well as generalized epilepsy and some cases of focal epilepsy as well. The fact that both these disorders are treated with anti-epileptic drugs (AEDs) strongly supports common underlying mechanisms. This review has been compiled with an aim to explore the alterations in common genes involved in various pathways regulating neuronal hyperexcitability, a common risk factor for both these conditions. The avenue for future treatment strategies targeting common genes and molecular mechanisms has also been discussed.Entities:
Keywords: Comorbidities; Epilepsy; Genomics; Migraine
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Year: 2021 PMID: 33856647 DOI: 10.1007/s12035-021-02386-x
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590