Evidence map›Paper›PMID 25540902›Full record

ReviewCurrent opinion in pharmacology2015

The NMDA receptor 'glycine modulatory site' in schizophrenia: D-serine, glycine, and beyond.

Darrick T Balu, Joseph T Coyle

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
14.7field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 206 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Neurophysiological Effects of Bitopertin in Schizophrenia.Journal of clinical psychopharmacology · 2017
    Trial
  5. Review
  6. UntargetedTranslational psychiatry · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Acetylcarnitine in cerebrospinal fluid and blood as a protective factor for neuromyelitis optica spectrum disorders: a mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Impact of Serine Racemase Deletion on Nicotine Discrimination.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2024
    Article
  20. Article

55 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

2 authors at 1 institution in 1 country.

Darrick T BaluDepartment of Psychiatry, Harvard Medical School, Boston, MA 02115, USA; Laboratory for Psychiatric and Molecular Neuroscience, McLean Hospital, Belmont, MA 02478, USA.
Joseph T CoyleDepartment of Psychiatry, Harvard Medical School, Boston, MA 02115, USA; Laboratory for Psychiatric and Molecular Neuroscience, McLean Hospital, Belmont, MA 02478, USA. Electronic address: joseph_coyle@hms.harvard.edu.
McLean Hospital · US

Funding

NMDA RECEPTOR FUNCTION IN SCHIZOPHRENIAP50MH060450 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 2000 to 2010
$15.4M
PSYCHOSIS AND BRAIN GLUTAMATER01MH051290 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 1994 to 2017
$5.0M
Drug Abuse, Schizophrenia, NMDA ReceptorR21DA035427 · NIDA · MCLEAN HOSPITAL · PI COYLE, JOSEPH T. · 2013 to 2014
$435k
NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniK99MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2013 to 2014
$230k
NIDA NIH HHS R21 DA035427NIMH NIH HHS 1K99MH099252-01A1NIMH NIH HHS K99 MH099252NIMH NIH HHS P50 MH060450NIMH NIH HHS P50MH0G0450NIMH NIH HHS R01 MH051290NIMH NIH HHS R01MH05190
6 · The paper itself

Abstract

Schizophrenia is a severe psychiatric illness that is characterized by reduced cortical connectivity, for which the underlying biological and genetic causes are not well understood. Although the currently approved antipsychotic drug treatments, which primarily modulate dopaminergic function, are effective at reducing positive symptoms (i.e. delusions and hallucinations), they do little to improve the disabling cognitive and negative (i.e. anhedonia) symptoms of patients with schizophrenia. This review details the recent genetic and neurobiological findings that link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiology of schizophrenia. It also highlights potential treatment strategies that augment NMDA receptor function to treat the synaptic deficits and cognitive impairments.

Indexed as

AnimalsAntipsychotic AgentsCognition DisordersDopamineGlycineHumansReceptors, N-Methyl-D-AspartateSchizophreniaSerineSynapsesAntipsychotic AgentsDopamineGlycineReceptors, N-Methyl-D-AspartateSerine

Identifiers

PMID25540902
PMCPMC4805108
OpenAlexW1996473902

What OpenQuestion holds

Textmetadata
LicenceTDM
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.