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Gene expression in human brain implicates sexually dimorphic pathways in autism spectrum disorders

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  • Donna M. Werling

    (Center for Neurobehavioral Genetics, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles)

  • Neelroop N. Parikshak

    (Center for Neurobehavioral Genetics, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles)

  • Daniel H. Geschwind

    (Center for Neurobehavioral Genetics, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles
    Program in Neurogenetics, David Geffen School of Medicine, University of California, Los Angeles
    Center for Autism Research and Treatment, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles
    David Geffen School of Medicine, University of California, Los Angeles)

Abstract

Autism spectrum disorder (ASD) is more prevalent in males, and the mechanisms behind this sex-differential risk are not fully understood. Two competing, but not mutually exclusive, hypotheses are that ASD risk genes are sex-differentially regulated, or alternatively, that they interact with characteristic sexually dimorphic pathways. Here we characterized sexually dimorphic gene expression in multiple data sets from neurotypical adult and prenatal human neocortical tissue, and evaluated ASD risk genes for evidence of sex-biased expression. We find no evidence for systematic sex-differential expression of ASD risk genes. Instead, we observe that genes expressed at higher levels in males are significantly enriched for genes upregulated in post-mortem autistic brain, including astrocyte and microglia markers. This suggests that it is not sex-differential regulation of ASD risk genes, but rather naturally occurring sexually dimorphic processes, potentially including neuron–glial interactions, that modulate the impact of risk variants and contribute to the sex-skewed prevalence of ASD.

Suggested Citation

  • Donna M. Werling & Neelroop N. Parikshak & Daniel H. Geschwind, 2016. "Gene expression in human brain implicates sexually dimorphic pathways in autism spectrum disorders," Nature Communications, Nature, vol. 7(1), pages 1-11, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10717
    DOI: 10.1038/ncomms10717
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    Cited by:

    1. Marlou Mackus & Deborah De Kruijff & Leila S. Otten & Aletta D. Kraneveld & Johan Garssen & Joris C. Verster, 2017. "Differential Gender Effects in the Relationship between Perceived Immune Functioning and Autistic Traits," IJERPH, MDPI, vol. 14(4), pages 1-6, April.
    2. Hyosang Kim & Doyoun Kim & Yisul Cho & Kyungdeok Kim & Junyeop Daniel Roh & Yangsik Kim & Esther Yang & Seong Soon Kim & Sunjoo Ahn & Hyun Kim & Hyojin Kang & Yongchul Bae & Eunjoon Kim, 2022. "Early postnatal serotonin modulation prevents adult-stage deficits in Arid1b-deficient mice through synaptic transcriptional reprogramming," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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