Evidence map›Paper›PMID 27130657›Full record

ReviewTrends in neurosciences2016

NMDA Receptor Internalization by Autoantibodies: A Reversible Mechanism Underlying Psychosis?

Joseph C Masdeu, Josep Dalmau, Karen F Berman

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Trends in neurosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03971487 (Ocrelizumab for Psychoses Possibly Caused by Synaptic Autoimmunity), which is not on this map. Cited by 49 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 3 pooled it
8.1field-weighted citation impact, top 2% 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.

NCT03971487 phase1 / phase2recruitingnot on this mapstarted 2019, after this paper: background citation

Ocrelizumab for Psychoses Possibly Caused by Synaptic Autoimmunity

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2019 to 2028Enrolled40ConditionsSchizo-Affective Type of Psychosis, SchizophreniaArmsPsychosis and cognitive assessments, Physical and neuro-cognitive evaluations, Safety labs and electrocardiogram, Ocrelizumab infusion
3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
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  7. Review
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  14. Observational
  15. Article
  16. Myelinating Co-Culture as a Model to Study Anti-NMDAR Neurotoxicity.International journal of molecular sciences · 2022
    Article
  17. Article
  18. Review
  19. Observational
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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

3 authors at 3 institutions in 2 countries.

Joseph C MasdeuHouston Methodist Neurological Institute and Department of Neurology, Weill Cornell Medical College, Houston, TX 77030, USA. Electronic address: jcmasdeu@houstonmethodist.org.
Josep DalmauICREA-IDIBAPS, Hospital Clinic, Service of Neurology, University of Barcelona, Barcelona, Spain; Department of Neurology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Karen F BermanClinical and Translational Neuroscience Branch, National Institutes of Health, NIMH Intramural Research Program, Bethesda, MD 20892, USA.
Cornell University · USNational Institutes of Health · USUniversitat de Barcelona · ES

Funding

Imaging of Neuropsychiatric Disorders with Developmental and Genetic MechanismsZIAMH002652 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI BERMAN, KAREN FAITH · 2009 to 2025
$17.3M
Multimodal Imaging: Genetic and Environmental Effects in NeuropsychiatryZIAMH002942 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI BERMAN, KAREN FAITH · 2013 to 2022
$12.2M
Paraneoplastic Disorders of the CNS: Autoantigen ProfilingR01NS077851 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI DALMAU, JOSEP O. · 2011 to 2015
$1.9M
Autoimmunity Against Novel Antigens in Neuropsychiatric DysfunctionR01MH094741 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI BALICE-GORDON, RITA J., DALMAU, JOSEP O. · 2011 to 2014
$1.3M
NIMH NIH HHS R01 MH094741NINDS NIH HHS R01 NS077851
6 · The paper itself

Abstract

Since the early 1990s it has been postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in brain networks supporting perception and cognition underlies schizophrenic psychosis. Recently, NMDA receptor hypofunction was described in patients with psychotic manifestations who exhibited autoantibodies binding the GluN1 subunit of the receptor, and who improved when the level of these antibodies was lowered by immunomodulation. In this disorder, NMDA receptor antibodies decrease the availability of NMDA receptors by internalizing them. In this opinion article, we review this mechanism as well as data supporting or refuting the possibility that this disorder or similar autoimmune disorders affecting synaptic proteins, which are therefore treatable with immunomodulation, could account for some cases of idiopathic psychosis. We also suggest methodological approaches to clarify this issue.

Indexed as

antibodiesimmunotherapyNMDA receptorpsychosisschizophreniasynapsis

Identifiers

PMID27130657
PMCPMC5913742
OpenAlexW2343055661

What OpenQuestion holds

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Registered trials

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.