IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms10717.html
   My bibliography  Save this article

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

Author

Listed:
  • 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
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms10717
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms10717?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Paolo Manghi & Michele Filosi & Moreno Zolfo & Lucas G. Casten & Albert Garcia-Valiente & Stefania Mattevi & Vitor Heidrich & Davide Golzato & Samuel Perini & Andrew M. Thomas & Simone Montalbano & Sa, 2024. "Large-scale metagenomic analysis of oral microbiomes reveals markers for autism spectrum disorders," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. 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.
    3. 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.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10717. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.