Evidence map›Paper›PMID 21210221›Full record

ArticleNeurochemical research2011

Targeting of glycine site on NMDA receptor as a possible new strategy for autism treatment.

Ahmad Ghanizadeh

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (NaInternational journal of environmental research and public health · 2019
    Review
  6. Review
  7. Article
  8. Article
  9. Glycine-dependent activation of NMDA receptors.The Journal of general physiology · 2015
    Article
  10. Review
  11. N-acetylcysteine for treatment of autism, a case report.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2012
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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

1 author at 1 institution in 1 country.

Ahmad GhanizadehResearch Center for Psychiatry and Behavioral Sciences, Department of Psychiatry, Hafez Hospital, Shiraz University of Medical Sciences, Shiraz, Iran. ghanizad@sina.tums.ac.ir
Hafez Hospital · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exact pathophysiology of the neurodevelopment disorder of autism is not clear and there is not any curative approach for it. There is only one FDA-approved medication for its management. Therefore, providing of novel treatments is highly required. The hypofunction of GABAergic system and glutamate toxicity are generally believed to have a causal role for autism. The antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.

Indexed as

Autistic DisorderGlycineHumansReceptors, N-Methyl-D-AspartateGlycineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21210221
OpenAlexW2089662966

What OpenQuestion holds

Textmetadata
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.