Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.

High titers of anti-NMDAR1 autoantibodies in brain cause anti-NMDAR1 encephalitis that displays psychiatric symptoms of schizophrenia and/or other psychiatric disorders in addition to neurological symptoms. Low titers of anti-NMDAR1 autoantibodies are reported in the blood of a subset of the general...

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Autores principales:	William Yue, Sorana Caldwell, Victoria Risbrough, Susan Powell, Xianjin Zhou
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4e7f2605b5ac49ae80248d56a7bbebb0
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spelling	oai:doaj.org-article:4e7f2605b5ac49ae80248d56a7bbebb02021-12-02T20:08:35ZChronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.1932-620310.1371/journal.pone.0256972https://doaj.org/article/4e7f2605b5ac49ae80248d56a7bbebb02021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0256972https://doaj.org/toc/1932-6203High titers of anti-NMDAR1 autoantibodies in brain cause anti-NMDAR1 encephalitis that displays psychiatric symptoms of schizophrenia and/or other psychiatric disorders in addition to neurological symptoms. Low titers of anti-NMDAR1 autoantibodies are reported in the blood of a subset of the general human population and psychiatric patients. Since ~0.1-0.2% of blood circulating antibodies cross the blood-brain barriers and antibodies can persist for months and years in human blood, it is important to investigate whether chronic presence of these blood circulating anti-NMDAR1 autoantibodies may impair human cognitive functions and contribute to the development of psychiatric symptoms. Here, we generated mice carrying low titers of anti-NMDAR1 autoantibodies in blood against a single antigenic epitope of mouse NMDAR1. Mice carrying the anti-NMDAR1 autoantibodies are healthy and display no differences in locomotion, sensorimotor gating, and contextual memory compared to controls. Chronic presence of the blood circulating anti-NMDAR1 autoantibodies, however, is sufficient to impair T-maze spontaneous alternation in the integrity of blood-brain barriers across all 3 independent mouse cohorts, indicating a robust cognitive deficit in spatial working memory and/or novelty detection. Our studies implicate that chronic presence of low titers of blood circulating anti-NMDAR1 autoantibodies may impair cognitive functions in both the general healthy human population and psychiatric patients.William YueSorana CaldwellVictoria RisbroughSusan PowellXianjin ZhouPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 9, p e0256972 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q William Yue Sorana Caldwell Victoria Risbrough Susan Powell Xianjin Zhou Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
description	High titers of anti-NMDAR1 autoantibodies in brain cause anti-NMDAR1 encephalitis that displays psychiatric symptoms of schizophrenia and/or other psychiatric disorders in addition to neurological symptoms. Low titers of anti-NMDAR1 autoantibodies are reported in the blood of a subset of the general human population and psychiatric patients. Since ~0.1-0.2% of blood circulating antibodies cross the blood-brain barriers and antibodies can persist for months and years in human blood, it is important to investigate whether chronic presence of these blood circulating anti-NMDAR1 autoantibodies may impair human cognitive functions and contribute to the development of psychiatric symptoms. Here, we generated mice carrying low titers of anti-NMDAR1 autoantibodies in blood against a single antigenic epitope of mouse NMDAR1. Mice carrying the anti-NMDAR1 autoantibodies are healthy and display no differences in locomotion, sensorimotor gating, and contextual memory compared to controls. Chronic presence of the blood circulating anti-NMDAR1 autoantibodies, however, is sufficient to impair T-maze spontaneous alternation in the integrity of blood-brain barriers across all 3 independent mouse cohorts, indicating a robust cognitive deficit in spatial working memory and/or novelty detection. Our studies implicate that chronic presence of low titers of blood circulating anti-NMDAR1 autoantibodies may impair cognitive functions in both the general healthy human population and psychiatric patients.
format	article
author	William Yue Sorana Caldwell Victoria Risbrough Susan Powell Xianjin Zhou
author_facet	William Yue Sorana Caldwell Victoria Risbrough Susan Powell Xianjin Zhou
author_sort	William Yue
title	Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
title_short	Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
title_full	Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
title_fullStr	Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
title_full_unstemmed	Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.
title_sort	chronic presence of blood circulating anti-nmdar1 autoantibodies impairs cognitive function in mice.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/4e7f2605b5ac49ae80248d56a7bbebb0
work_keys_str_mv	AT williamyue chronicpresenceofbloodcirculatingantinmdar1autoantibodiesimpairscognitivefunctioninmice AT soranacaldwell chronicpresenceofbloodcirculatingantinmdar1autoantibodiesimpairscognitivefunctioninmice AT victoriarisbrough chronicpresenceofbloodcirculatingantinmdar1autoantibodiesimpairscognitivefunctioninmice AT susanpowell chronicpresenceofbloodcirculatingantinmdar1autoantibodiesimpairscognitivefunctioninmice AT xianjinzhou chronicpresenceofbloodcirculatingantinmdar1autoantibodiesimpairscognitivefunctioninmice
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Chronic presence of blood circulating anti-NMDAR1 autoantibodies impairs cognitive function in mice.

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