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Sci Rep. 2018 Jul 17;8(1):10757. doi: 10.1038/s41598-018-28986-7.

A monocyte gene expression signature in the early clinical course of Parkinson's disease.

Author information

1
Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander Universität (FAU) Erlangen-Nürnberg, 91054, Erlangen, Germany. jschlachetzki@ucsd.edu.
2
Department of Cellular and Molecular Medicine, University of California, San Diego at La Jolla, CA, 92093-0651, USA. jschlachetzki@ucsd.edu.
3
Department of Stem Cell Biology, FAU Erlangen-Nürnberg, 91054, Erlangen, Germany.
4
Department of Cellular and Molecular Medicine, University of California, San Diego at La Jolla, CA, 92093-0651, USA.
5
Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA, 94720-3200, USA.
6
Department of Molecular Medicine, Centre de Recherche du CHU de Québec - Université Laval, Québec, G1V 4G2, Canada.
7
Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander Universität (FAU) Erlangen-Nürnberg, 91054, Erlangen, Germany. juergen.winkler@uk-erlangen.de.

Abstract

Microglia are the main immune cells of the brain and express a large genetic pattern of genes linked to Parkinson's disease risk alleles. Monocytes like microglia are myeloid-lineage cells, raising the questions of the extent to which they share gene expression with microglia and whether they are already altered early in the clinical course of the disease. To decipher a monocytic gene expression signature in Parkinson's disease, we performed RNA-seq and applied the two-sample Kolmogorov-Smirnov test to identify differentially expressed genes between controls and patients with Parkinson's disease and changes in gene expression variability and dysregulation. The gene expression profiles of normal human monocytes and microglia showed a plethora of differentially expressed genes. Additionally, we identified a distinct gene expression pattern of monocytes isolated from Parkinson's disease patients at an early disease stage compared to controls using the Kolmogorov-Smirnov test. Differentially expressed genes included genes involved in immune activation such as HLA-DQB1, MYD88, REL, and TNF-α. Our data suggest that future studies of distinct leukocyte subsets are warranted to identify possible surrogate biomarkers and may lead to the identification of novel interventions early in the disease course.

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