The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor

N-methyl-D-aspartate receptors (NMDAR) play a key role in brain development and function, including contributing to the pathogenesis of many neurological disorders. Immunization against the GluN1 subunit of the NMDAR and the production of GluN1 antibodies is associated with neuroprotective and seizu...

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Detalles Bibliográficos
Autor principal: Young, Deborah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Neurology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347966/
https://www.ncbi.nlm.nih.gov/pubmed/32719654
http://dx.doi.org/10.3389/fneur.2020.00635
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author Young, Deborah
author_facet Young, Deborah
author_sort Young, Deborah
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description N-methyl-D-aspartate receptors (NMDAR) play a key role in brain development and function, including contributing to the pathogenesis of many neurological disorders. Immunization against the GluN1 subunit of the NMDAR and the production of GluN1 antibodies is associated with neuroprotective and seizure-protective effects in rodent models of stroke and epilepsy, respectively. Whilst these data suggest the potential for the development of GluN1 antibody therapy, paradoxically GluN1 autoantibodies in humans are associated with the pathogenesis of the autoimmune disease anti-NMDA receptor encephalitis. This review discusses possible reasons for the differential effects of GluN1 antibodies on NMDAR physiology that could contribute to these phenotypes.
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spelling pubmed-73479662020-07-26 The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor Young, Deborah Front Neurol Neurology N-methyl-D-aspartate receptors (NMDAR) play a key role in brain development and function, including contributing to the pathogenesis of many neurological disorders. Immunization against the GluN1 subunit of the NMDAR and the production of GluN1 antibodies is associated with neuroprotective and seizure-protective effects in rodent models of stroke and epilepsy, respectively. Whilst these data suggest the potential for the development of GluN1 antibody therapy, paradoxically GluN1 autoantibodies in humans are associated with the pathogenesis of the autoimmune disease anti-NMDA receptor encephalitis. This review discusses possible reasons for the differential effects of GluN1 antibodies on NMDAR physiology that could contribute to these phenotypes. Frontiers Media S.A. 2020-07-03 /pmc/articles/PMC7347966/ /pubmed/32719654 http://dx.doi.org/10.3389/fneur.2020.00635 Text en Copyright © 2020 Young. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neurology
Young, Deborah
The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title_full The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title_fullStr The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title_full_unstemmed The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title_short The NMDA Receptor Antibody Paradox: A Possible Approach to Developing Immunotherapies Targeting the NMDA Receptor
title_sort nmda receptor antibody paradox: a possible approach to developing immunotherapies targeting the nmda receptor
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347966/
https://www.ncbi.nlm.nih.gov/pubmed/32719654
http://dx.doi.org/10.3389/fneur.2020.00635
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