bioRxiv · 10.1101/2021.08.15.456398
In silico Analysis of Transcriptomic Profiling and Affected Biological pathways in Multiple Sclerosis
Abstract
Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease that is widely associated with Grey and white matter degradation due to the demyelination of axons. Thus exposing the underlying causes of this condition can lead to a novel treatment approach for Multiple Sclerosis. The total RNA microarray processed data from GEO for Multiple sclerotic patients was comprehensively analyzed to find out underlying differences between Grey Matter lesions (GML), Normal appearing Grey Matter (NAGM), and Control Grey matter at the transcriptomics level. Thus, in the current study, we performed various bioinformatics analyses on transcriptional profiles of 184 samples including 105 NAGM, 37 GML, and 42 Controls obtained from the NCBI-Bio project (PRJNA543111). First, exploratory data analysis based on gene expression data using principal component analysis (PCA) depicted distinct patterns between GML and CG samples. Subsequently, the Welchs T-test differential gene expression analysis identified 15,525 significantly differentially expressed genes (p.adj value <0.05, Fold change(>=+/-1.5) between these conditions. This study reveals the genes like CREB3L2, KIF5B, WIPI1, EP300, NDUFA1, ATG101, AND TAF4 as the key features that may substantially contribute to loss of cognitive functions in Multiple sclerosis and several other neurodegenerative disorders. Further, this study also proposes genes associated with Huntingtons disease in Multiple sclerotic patients. Eventually, the results presented here reveal new insights into MS and how it affects the development of male primary sexual characteristics.
Explore related subjects
Keep this discovery
Explore connections, maps & timelines
Vaja, R. D., Kaur, H., Mazumder, M., Brodsky, E.. 2021-08-17. In silico Analysis of Transcriptomic Profiling and Affected Biological pathways in Multiple Sclerosis. https://doi.org/10.1101/2021.08.15.456398
Cite the original work for its findings. Save a collection to share your selection of sources.