Transcriptomic differences in MSA clinical variants

Sci Rep. 2020 Jun 25;10(1):10310. doi: 10.1038/s41598-020-66221-4.

Abstract

Background: Multiple system atrophy (MSA) is a rare oligodendroglial synucleinopathy of unknown etiopathogenesis including two major clinical variants with predominant parkinsonism (MSA-P) or cerebellar dysfunction (MSA-C).

Objective: To identify novel disease mechanisms we performed a blood transcriptomic study investigating differential gene expression changes and biological process alterations in MSA and its clinical subtypes.

Methods: We compared the transcriptome from rigorously gender and age-balanced groups of 10 probable MSA-P, 10 probable MSA-C cases, 10 controls from the Catalan MSA Registry (CMSAR), and 10 Parkinson Disease (PD) patients.

Results: Gene set enrichment analyses showed prominent positive enrichment in processes related to immunity and inflammation in all groups, and a negative enrichment in cell differentiation and development of the nervous system in both MSA-P and PD, in contrast to protein translation and processing in MSA-C. Gene set enrichment analysis using expression patterns in different brain regions as a reference also showed distinct results between the different synucleinopathies.

Conclusions: In line with the two major phenotypes described in the clinic, our data suggest that gene expression and biological processes might be differentially affected in MSA-P and MSA-C. Future studies using larger sample sizes are warranted to confirm these results.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Case-Control Studies
  • Cerebellar Diseases / blood
  • Cerebellar Diseases / diagnosis*
  • Cerebellar Diseases / genetics
  • Diagnosis, Differential
  • Female
  • Gene Expression Profiling
  • Humans
  • Male
  • Middle Aged
  • Multiple System Atrophy / blood
  • Multiple System Atrophy / diagnosis*
  • Multiple System Atrophy / genetics
  • Parkinson Disease / blood
  • Parkinson Disease / diagnosis*
  • Parkinson Disease / genetics
  • Transcriptome*