Transcriptome analysis reveals dysregulation of innate immune response genes and neuronal activity-dependent genes in autism

Simone Gupta, Shannon E. Ellis, Foram N. Ashar, Anna Moes, Joel S. Bader, Jianan Zhan, Andrew B. West () and Dan E. Arking ()
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Simone Gupta: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Shannon E. Ellis: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Foram N. Ashar: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Anna Moes: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Joel S. Bader: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Jianan Zhan: Johns Hopkins University School of Medicine
Andrew B. West: University of Alabama at Birmingham
Dan E. Arking: McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine

Nature Communications, 2014, vol. 5, issue 1, 1-8

Abstract: Abstract Recent studies of genomic variation associated with autism have suggested the existence of extreme heterogeneity. Large-scale transcriptomics should complement these results to identify core molecular pathways underlying autism. Here we report results from a large-scale RNA sequencing effort, utilizing region-matched autism and control brains to identify neuronal and microglial genes robustly dysregulated in autism cortical brain. Remarkably, we note that a gene expression module corresponding to M2-activation states in microglia is negatively correlated with a differentially expressed neuronal module, implicating dysregulated microglial responses in concert with altered neuronal activity-dependent genes in autism brains. These observations provide pathways and candidate genes that highlight the interplay between innate immunity and neuronal activity in the aetiology of autism.

Date: 2014
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DOI: 10.1038/ncomms6748

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