Postnatal immune activation causes social deficits in a mouse model of tuberous sclerosis: Role of microglia and clinical implications

Author:

López-Aranda Manuel F.1ORCID,Chattopadhyay Ishanu23ORCID,Boxx Gayle M.4ORCID,Fraley Elizabeth R.5,Silva Tawnie K.1ORCID,Zhou Miou1ORCID,Phan Miranda1,Herrera Isaiah1ORCID,Taloma Sunrae1ORCID,Mandanas Rochelle1ORCID,Bach Karen1ORCID,Gandal Michael6ORCID,Geschwind Daniel H.6ORCID,Cheng Genhong4ORCID,Rzhetsky Andrey237ORCID,White Stephanie A.5ORCID,Silva Alcino J.1ORCID

Affiliation:

1. Departments of Neurobiology, Psychology, and Psychiatry, Integrative Center for Learning and Memory, and Brain Research Institute, University of California, Los Angeles, Los Angeles, CA, USA.

2. Department of Medicine and Human Genetics, Section of Computational Biomedicine and Biomedical Data Science, and Institute for Genomics and Systems Biology, University of Chicago, Chicago, IL, USA.

3. Department of Medicine, University of Chicago, Chicago, IL, USA.

4. Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA.

5. Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.

6. Department of Neurology, Center for Autism Research and Treatment, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

7. Department of Human Genetics, University of Chicago, Chicago, IL, USA.

Abstract

Postnatal immune activation leads to social deficits in a mouse model of TSC by abnormal interferon production in microglia.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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