Publications by authors named "E Cuenca-Leon"

Background: Cortical spreading depolarization, the cause of migraine aura, is a short-lasting depolarization wave that moves across the brain cortex, transiently suppressing neuronal activity. Prophylactic treatments for migraine, such as topiramate or valproate, reduce the number of cortical spreading depression events in rodents.

Objective: To investigate whether cortical spreading depolarization with and without chronic treatment with topiramate or valproate affect the DNA methylation of the cortex.

View Article and Find Full Text PDF
Article Synopsis
  • A study investigated the genetic overlap between 25 brain disorders using data from over 1.2 million individuals, finding that psychiatric disorders share more genetic risk compared to neurological disorders, which seem more distinct.
  • The research identified significant relationships between these disorders and various cognitive measures, suggesting shared underlying traits.
  • Simulations were conducted to understand how factors like sample size and diagnosis accuracy influence genetic correlations, emphasizing the role of common genetic variations in the risk of brain disorders.
View Article and Find Full Text PDF

Objective To study the position of hemiplegic migraine in the clinical spectrum of migraine with aura and to reveal the importance of CACNA1A, ATP1A2 and SCN1A in the development of hemiplegic migraine in Finnish migraine families. Methods The International Classification of Headache Disorders 3rd edition criteria were used to determine clinical characteristics and occurrence of hemiplegic migraine, based on detailed questionnaires, in a Finnish migraine family collection consisting of 9087 subjects. Involvement of CACNA1A, ATP1A2 and SCN1A was studied using whole exome sequencing data from 293 patients with hemiplegic migraine.

View Article and Find Full Text PDF

Episodic ataxia is an autosomal dominant ion channel disorder characterized by episodes of imbalance and incoordination. The disease is genetically heterogeneous and is classified as episodic ataxia type 2 (EA2) when it is caused by a mutation in the CACNA1A gene, encoding the α subunit of the P/Q-type voltage-gated calcium channel Ca2.1.

View Article and Find Full Text PDF