Evidence map›Paper›PMID 28763062›Full record

ArticleTranslational psychiatry2017

Pathogen-mediated NMDA receptor autoimmunity and cellular barrier dysfunction in schizophrenia.

G Kannan, K L Gressitt, S Yang, C R Stallings, E Katsafanas, L A Schweinfurth, C L G Savage, M B Adamos, K M Sweeney, A E Origoni and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 52 citations in OpenAlex.

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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

17 authors at 5 institutions in 4 countries.

G KannanDepartment of Psychiatry, Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
K L GressittStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
S YangStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
C R StallingsSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
E KatsafanasSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
L A SchweinfurthSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
C L G SavageSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
M B AdamosSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
K M SweeneySheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
A E OrigoniSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
S KhushalaniSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
S BahnDepartment of Chemical Engineering and Biotechnology, University of Cambridge, Cambridge, UK.
F M LewekeDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
F B DickersonSheppard Pratt Health System, Stanley Research Program, Baltimore, MD, USA.
R H YolkenStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
M V PletnikovDepartment of Psychiatry, Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
E G SeveranceStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Sheppard Pratt Health System · USJohns Hopkins Medicine · USJohns Hopkins University · USHeidelberg University · DEUniversity of Cambridge · GB

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
NIGMS NIH HHS T32 GM008752NIMH NIH HHS P50 MH094268
6 · The paper itself

Abstract

Autoantibodies that bind the N-methyl-D-aspartate receptor (NMDAR) may underlie glutamate receptor hypofunction and related cognitive impairment found in schizophrenia. Exposure to neurotropic pathogens can foster an autoimmune-prone environment and drive systemic inflammation leading to endothelial barrier defects. In mouse model cohorts, we demonstrate that infection with the protozoan parasite, Toxoplasma gondii, caused sustained elevations of IgG class antibodies to the NMDAR in conjunction with compromised blood-gut and blood-brain barriers. In human cohorts, NMDAR IgG and markers of barrier permeability were significantly associated with T. gondii exposure in schizophrenia compared with controls and independently of antipsychotic medication. Combined T. gondii and NMDAR antibody seropositivity in schizophrenia resulted in higher degrees of cognitive impairment as measured by tests of delayed memory. These data underscore the necessity of disentangling the heterogeneous pathophysiology of schizophrenia so that relevant subsets eligible for NMDAR-related treatment can be identified. Our data aid to reconcile conflicting reports regarding a role of pathological NMDAR autoantibodies in this disorder.

Indexed as

AdultAnimalsAutoantibodiesAutoimmunityFemaleHumansMaleMiceMiddle AgedReceptors, N-Methyl-D-AspartateSchizophreniaToxoplasmaYoung AdultAutoantibodiesReceptors, N-Methyl-D-Aspartate

Identifiers

PMID28763062
PMCPMC5611729
OpenAlexW2739687817

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.