Evidence map›Paper›PMID 31293459›Full record

ReviewFrontiers in psychiatry2019

Autism Associated With Anti-NMDAR Encephalitis: Glutamate-Related Therapy.

Ruu-Fen Tzang, Chuan-Hsin Chang, Yue-Cune Chang, Hsien-Yuan Lane

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. The Neuroimmunology of Autism.Molecular neurobiology · 2025
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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

4 authors at 4 institutions in 1 country.

Ruu-Fen TzangDepartment of Psychiatry, Mackay Memorial Hospital, Taipei, Taiwan.
Chuan-Hsin ChangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
Yue-Cune ChangDepartment of Mathematics, Tamkang University, Taipei, Taiwan.
Hsien-Yuan LaneDepartment of Psychiatry, China Medical University Hospital, Taichung, Taiwan.
Agricultural Biotechnology Research Center, Academia Sinica · TWChina Medical University Hospital · TWMackay Memorial Hospital · TWTamkang University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this review is to correlate autism with autoimmune dysfunction in the absence of an explanation for the etiology of autism spectrum disorder. The anti-N-methyl-D-aspartate receptor (anti-NMDAR) autoantibody is a typical synaptic protein that can bind to synaptic NMDA glutamate receptors, leading to dysfunctional glutamate neurotransmission in the brain that manifests as psychiatric symptoms (psychosis, hallucinations, and personality changes). Detection of autoantibodies, cytokines, decreased lymphocytes, serum immunoglobulin level imbalance, T-cell mediated immune profile, maternal infection history, and children's infection history can all be vital biological markers of autoimmune autism. Diagnosing autoimmune encephalitis sooner can increase the effectiveness of curative treatments-such as immune therapy or immune modulatory therapy-that may prevent the long-term consequence of being misdiagnosed with autism spectrum disorder. Glutamate therapy primarily normalizes glutamate neurotransmission and can be a new add-on intervention alongside antipsychotics for treating autoimmune autism.

Indexed as

anti-N-methyl-D-aspartate receptor encephalitisautoimmune autismdysfunctional glutamate neurotransmissionglutamate-related therapyimmune therapy

Identifiers

PMID31293459
PMCPMC6598425
OpenAlexW2951212001

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.