Evidence map›Paper›PMID 32089545›Full record

ArticleMolecular psychiatry2021

Multiple inducers and novel roles of autoantibodies against the obligatory NMDAR subunit NR1: a translational study from chronic life stress to brain injury.

Hong Pan, Agnes A Steixner-Kumar, Anna Seelbach, Nadine Deutsch, Anja Ronnenberg, Daniel Tapken, Nico von Ahsen, Marina Mitjans, Hans Worthmann, Ralf Trippe and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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  16. Global Landscape of Encephalitis: Key Priorities to Reduce Future Disease Burden.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 6 institutions in 1 country.

Hong PanClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Agnes A Steixner-KumarClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0001-7913-2716
Anna SeelbachClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-7908-7369
Nadine DeutschDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Anja RonnenbergClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Daniel TapkenDepartment of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.
Nico von AhsenInstitute of Clinical Chemistry, University Medical Center Göttingen, Göttingen, Germany.
Marina MitjansClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Hans WorthmannDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Ralf TrippeDepartment of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.
Christina Klein-SchmidtDepartment of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.
Nadine SchopfClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Kristin RentzschInstitute for Experimental Immunology, Euroimmun, Lübeck, Germany.
Martin BegemannClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Jürgen WienandsInstitute for Cellular and Molecular Immunology, Georg August University, Göttingen, Germany.
Winfried StöckerInstitute for Experimental Immunology, Euroimmun, Lübeck, Germany.
Karin WeissenbornDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Michael HollmannDepartment of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.
Klaus-Armin NaveNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0001-8724-9666
Fred LühderInstitute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany.
Hannelore EhrenreichClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany. ehrenreich@em.mpg.de.ORCID http://orcid.org/0000-0001-8371-5711
Max Planck Institute of Experimental Medicine · DERuhr University Bochum · DEMedizinische Hochschule Hannover · DEUniversitätsmedizin Göttingen · DEEuroimmun Medizinische Labordiagnostika (Germany) · DEUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circulating autoantibodies (AB) of different immunoglobulin classes (IgM, IgA, and IgG), directed against the obligatory N-methyl-D-aspartate-receptor subunit NR1 (NMDAR1-AB), belong to the mammalian autoimmune repertoire, and appear with age-dependently high seroprevalence across health and disease. Upon access to the brain, they can exert NMDAR-antagonistic/ketamine-like actions. Still unanswered key questions, addressed here, are conditions of NMDAR1-AB formation/boosting, intraindividual persistence/course in serum over time, and (patho)physiological significance of NMDAR1-AB in modulating neuropsychiatric phenotypes. We demonstrate in a translational fashion from mouse to human that (1) serum NMDAR1-AB fluctuate upon long-term observation, independent of blood-brain barrier (BBB) perturbation; (2) a standardized small brain lesion in juvenile mice leads to increased NMDAR1-AB seroprevalence (IgM + IgG), together with enhanced Ig-class diversity; (3) CTLA4 (immune-checkpoint) genotypes, previously found associated with autoimmune disease, predispose to serum NMDAR1-AB in humans; (4) finally, pursuing our prior findings of an early increase in NMDAR1-AB seroprevalence in human migrants, which implicated chronic life stress as inducer, we independently replicate these results with prospectively recruited refugee minors. Most importantly, we here provide the first experimental evidence in mice of chronic life stress promoting serum NMDAR1-AB (IgA). Strikingly, stress-induced depressive-like behavior in mice and depression/anxiety in humans are reduced in NMDAR1-AB carriers with compromised BBB where NMDAR1-AB can readily reach the brain. To conclude, NMDAR1-AB may have a role as endogenous NMDAR antagonists, formed or boosted under various circumstances, ranging from genetic predisposition to, e.g., tumors, infection, brain injury, and stress, altogether increasing over lifetime, and exerting a spectrum of possible effects, also including beneficial functions.

Indexed as

AutoantibodiesBrain InjuriesAnimalsBlood-Brain BarrierMiceReceptors, N-Methyl-D-AspartateSeroepidemiologic StudiesStress, PsychologicalAutoantibodiesReceptors, N-Methyl-D-Aspartate

Identifiers

PMID32089545
PMCPMC8440197
OpenAlexW3008145734

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.