Evidence map›Paper›PMID 27288082›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2016

The NMDA Receptor and Schizophrenia: From Pathophysiology to Treatment.

D T Balu

Abstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

152 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  9. Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026
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92 more citing papers are in PubMed but not listed here.

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.

D T BaluHarvard Medical School, Boston, MA, United States; McLean Hospital, Belmont, MA, United States. Electronic address: dbalu@mclean.harvard.edu.

Funding

NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniR00MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2015 to 2017
$726k
NIMH NIH HHS R00 MH099252
6 · The paper itself

Abstract

Schizophrenia is a severe mental illness that affects almost 1% of the population worldwide. Even though the etiology of schizophrenia is uncertain, it is believed to be a neurodevelopmental disorder that results from a combination of environmental insults and genetic vulnerabilities. Over the past 20 years, there has been a confluence of evidence from many research disciplines pointing to alterations in excitatory signaling, particularly involving hypofunction of the N-methyl-d-aspartate receptor (NMDAR), as a key contributor to the schizophrenia disease process. This review describes the structure-function relationship of the NMDAR channel and how the glycine modulatory site acts as an important regulator of its activity. In addition, this review highlights the genetic, pharmacologic, and biochemical evidence supporting the hypothesis that NMDAR hypofunction contributes to the pathophysiology of schizophrenia. Finally, this chapter highlights some of the most recent and promising pharmacological strategies that are designed to either, directly or indirectly, augment NMDAR function in an effort to treat the cognitive and negative symptoms of schizophrenia that are not helped by currently available medications.

Indexed as

Signal TransductionAnimalsHumansReceptors, N-Methyl-D-AspartateSchizophreniaReceptors, N-Methyl-D-AspartateCognitiond-serineGlycineMetabotropic glutamate receptor 5NMDA receptorSchizophreniaSerine racemaseα7 Nicotinic acetylcholine receptors

Identifiers

PMID27288082
PMCPMC5518924

What OpenQuestion holds

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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.