Cognitive impairment and autistic-like behaviour in SAPAP4-deficient mice View Full Text


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Article Info

DATE

2019-12

AUTHORS

Claudia Schob, Fabio Morellini, Ora Ohana, Lidia Bakota, Mariya V. Hrynchak, Roland Brandt, Marco D. Brockmann, Nicole Cichon, Henrike Hartung, Ileana L. Hanganu-Opatz, Vanessa Kraus, Sarah Scharf, Irm Herrmans-Borgmeyer, Michaela Schweizer, Dietmar Kuhl, Markus Wöhr, Karl J. Vörckel, Julia Calzada-Wack, Helmut Fuchs, Valérie Gailus-Durner, Martin Hrabě de Angelis, Craig C. Garner, Hans-Jürgen Kreienkamp, Stefan Kindler

ABSTRACT

In humans, genetic variants of DLGAP1-4 have been linked with neuropsychiatric conditions, including autism spectrum disorder (ASD). While these findings implicate the encoded postsynaptic proteins, SAPAP1-4, in the etiology of neuropsychiatric conditions, underlying neurobiological mechanisms are unknown. To assess the contribution of SAPAP4 to these disorders, we characterized SAPAP4-deficient mice. Our study reveals that the loss of SAPAP4 triggers profound behavioural abnormalities, including cognitive deficits combined with impaired vocal communication and social interaction, phenotypes reminiscent of ASD in humans. These behavioural alterations of SAPAP4-deficient mice are associated with dramatic changes in synapse morphology, function and plasticity, indicating that SAPAP4 is critical for the development of functional neuronal networks and that mutations in the corresponding human gene, DLGAP4, may cause deficits in social and cognitive functioning relevant to ASD-like neurodevelopmental disorders. More... »

PAGES

7

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41398-018-0327-z

    DOI

    http://dx.doi.org/10.1038/s41398-018-0327-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1111568186

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30664629


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