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Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

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Transcriptomic differences in MSA clinical variants.

Alexandra Pérez-Soriano^1,2,3, Magdalena Arnal Segura^3,4, Teresa Botta-Orfila^3,5

¹Parkinson's Disease & Movement Disorders Unit, Hospital Clínic/IDIBAPS/CIBERNED/European Reference Network for Rare Neurological Diseases (ERN-RND)/Institut de Neurociències, University of Barcelona, Catalonia, Spain.

Scientific Reports

|June 27, 2020

Summary

Multiple system atrophy (MSA) involves distinct gene expression changes in its parkinsonian (MSA-P) and cerebellar (MSA-C) subtypes. These findings suggest differing biological pathways contribute to MSA

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Area of Science:

Neuroscience
Genomics
Molecular Biology

Background:

Multiple system atrophy (MSA) is a rare, fatal neurodegenerative disorder affecting oligodendroglia.
It presents with two main clinical variants: MSA with predominant parkinsonism (MSA-P) and MSA with cerebellar dysfunction (MSA-C).
The underlying etiopathogenesis of MSA remains largely unknown.

Purpose of the Study:

To investigate novel disease mechanisms in MSA by analyzing blood transcriptomic data.
To identify differential gene expression and biological process alterations in MSA subtypes (MSA-P and MSA-C).

Main Methods:

Blood transcriptomic analysis was performed on small, balanced cohorts.
Participants included probable MSA-P (n=10), MSA-C (n=10), healthy controls (n=10), and Parkinson's Disease (PD) patients (n=10).
Gene set enrichment analyses were conducted to identify altered biological processes.

Main Results:

Immunity and inflammation pathways were upregulated across all MSA and PD groups.
Cell differentiation and nervous system development pathways were downregulated in MSA-P and PD.
Protein translation and processing pathways showed distinct alterations in MSA-C compared to MSA-P and PD.
Distinct gene expression patterns were observed between different synucleinopathies.

Conclusions:

Gene expression and biological processes appear to be differentially affected in MSA-P and MSA-C subtypes.
These findings suggest distinct molecular mechanisms underlying the clinical variants of MSA.
Larger sample sizes are needed to validate these preliminary results.