Abstract
Although dramatic progress has been achieved in the understanding and treatment of multiple sclerosis (MS) and ischemic stroke (IS), more precise and instructive support is required for further research. Recent large-scale genome-wide association studies (GWASs) have already revealed risk variants for IS and MS, but the common genetic etiology between MS and IS remains an unresolved issue. This research was designed to overlapping genes between MS and IS and unmask their transcriptional features. We designed a three-section analysis process. Firstly, we computed gene-based analyses of MS GWAS and IS GWAS data sets by VGEAS2. Secondly, overlapping genes of significance were identified in a meta-analysis using the Fisher’s procedure. Finally, we performed gene expression analyses to confirm transcriptional changes. We identified 24 shared genes with Bonferroni correction (Pcombined < 2.31E-04), and five (FOXP1, CAMK2G, CLEC2D, LBH, and SLC2A4RG) had significant expression differences in MS and IS gene expression omnibus data sets. These meaningful shared genes between IS and MS shed light on the underlying genetic etiologies shared by the diseases. Our results provide a basis for in-depth genomic studies of associations between MS and IS.
Highlights
Multiple sclerosis and ischemic stroke (IS) are two major neurological diseases with serious sequelae such as motor and/or sensory disabilities, cognitive impairment, and mental disorders (Compston and Coles, 2008; Johnson et al, 2016)
As environmental variants are complicated, the genetic variants are regarded as a possible direction to make progress in immune-related mechanisms and therapies
Pi is the P value of the genes, and k is the entire count of studies. x2 abides by a c2 distribution with 2k degrees of freedom (Begum et al, 2012)
Summary
Multiple sclerosis and IS are two major neurological diseases with serious sequelae such as motor and/or sensory disabilities, cognitive impairment, and mental disorders (Compston and Coles, 2008; Johnson et al, 2016). Multiple sclerosis is a chronic autoimmune disease in the CNS mainly characterized by demyelination in brain and spinal cord (Compston and Coles, 2008). As environmental variants are complicated, the genetic variants are regarded as a possible direction to make progress in immune-related mechanisms and therapies
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