Genetic Screening of Plasticity Regulating Nogo-Type Signaling Genes in Migraine.

Gabriella Smedfors,Andrea Carmine Belin,Caroline Ran,Tobias Karlsson,Franziska Liesecke,Lars Olson

doi:10.3390/brainsci10010005

Abstract

Migraine is the sixth most prevalent disease in the world and a substantial number of experiments have been conducted to analyze potential differences between the migraine brain and the healthy brain. Results from these investigations point to the possibility that development and aggravation of migraine may include grey matter plasticity. Nogo-type signaling is a potent plasticity regulating system in the CNS and consists of ligands, receptors, co-receptors and modulators with a dynamic age- and activity-related expression in cortical and subcortical regions. Here we investigated a potential link between migraine and five key Nogo-type signaling genes: RTN4, OMGP, MAG, RTN4R and LINGO1, by screening 15 single nucleotide polymorphisms (SNPs) within these genes. In a large Swedish migraine cohort (749 migraine patients and 4032 controls), using a logistic regression with sex as covariate, we found that there was no such association. In addition, a haplotype analysis was performed which revealed three haplotype blocks. These blocks had no significant association with migraine. However, to robustly conclude that Nogo-type genotypes signaling do not influence the prevalence of migraine, further studies are encouraged.

Highlights

IntroductionWhile primarily associated with a burdening, often pulsating headache, migraine is frequently accompanied by other symptoms of altered sensory function
Migraine is the sixth most prevalent disease in the world [1]
Nogo-type signaling involves a broad number of receptors, ligands, co-receptors and modulators

Summary

Introduction

While primarily associated with a burdening, often pulsating headache, migraine is frequently accompanied by other symptoms of altered sensory function. These symptoms vary in type, frequency and intensity between individuals. About one third of all migraine patients experience the phenomenon of aura. Migraine with aura indicates transient neurological symptoms prior to the headache, often visual and/or a sensation of numbing and weakness in various parts of the body [4,5]. The migraine aura appears to be the result of cortical spreading depression which, in turn, has been associated with increased inflammation and subsequent activation of trigeminal afferents known to cause pain [6].

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Conclusion