{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T02:17:05Z","timestamp":1777601825471,"version":"3.51.4"},"reference-count":104,"publisher":"MDPI AG","issue":"8","license":[{"start":{"date-parts":[[2020,8,7]],"date-time":"2020-08-07T00:00:00Z","timestamp":1596758400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JCM"],"abstract":"<jats:p>Recent studies indicate the existence of a maternal-autoantibody-related subtype of autism spectrum disorder (ASD). To date, a large number of studies have focused on describing patterns of brain-reactive serum antibodies in maternal-autoantibody-related (MAR) autism and some have described attempts to define the antigenic targets. This article describes evidence on MAR autism and the various autoantibodies that have been implicated. Among other possibilities, antibodies to neuronal surface protein Contactin Associated Protein 2 (CASPR2) have been found more frequently in mothers of children with neurodevelopmental disorders or autism, and two independent experimental studies have shown pathogenicity in mice. The N-methyl-D-aspartate receptor (NMDAR) is another possible target for maternal antibodies as demonstrated in mice. Here, we discuss the growing evidence, discuss issues regarding biomarker definition, and summarise the therapeutic approaches that might be used to reduce or prevent the transfer of pathogenic maternal antibodies.<\/jats:p>","DOI":"10.3390\/jcm9082564","type":"journal-article","created":{"date-parts":[[2020,8,10]],"date-time":"2020-08-10T07:25:03Z","timestamp":1597044303000},"page":"2564","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Maternal-Autoantibody-Related (MAR) Autism: Identifying Neuronal Antigens and Approaching Prospects for Intervention"],"prefix":"10.3390","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1511-2526","authenticated-orcid":false,"given":"Katya","family":"Marks","sequence":"first","affiliation":[{"name":"Medical Sciences Division, John Radcliffe Hospital, University of Oxford, OX3 9DU Oxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ester","family":"Coutinho","sequence":"additional","affiliation":[{"name":"Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King\u2019s College London, SE5 9RT London, UK"},{"name":"Medical Research Council Centre for Neurodevelopmental Disorders, King\u2019s College London, SE1 1UL London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angela","family":"Vincent","sequence":"additional","affiliation":[{"name":"Nuffield Department of Clinical Neurosciences and Weatherall Institute for Molecular Medicine, University of Oxford, OX3 9DS Oxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2020,8,7]]},"reference":[{"key":"ref_1","unstructured":"World Health Organization (2020, May 13). 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