Evidence map›Paper›PMID 39218136›Full record

ReviewBiological psychiatry2025

Finding the Right Dose: NMDA Receptor-Modulating Treatments for Cognitive and Plasticity Deficits in Schizophrenia and the Role of Pharmacodynamic Target Engagement.

Pejman Sehatpour, Joshua T Kantrowitz

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Serotonin type 3 receptor (5-HTNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Pooled it
  3. Trial
  4. Review
  5. Article
  6. Article
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  9. Article
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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

2 authors.

Pejman SehatpourNew York State Psychiatric Institute, New York, New York; College of Physicians and Surgeons, Columbia University, New York, New York; Nathan Kline Institute, Orangeburg, New York.
Joshua T KantrowitzNew York State Psychiatric Institute, New York, New York; College of Physicians and Surgeons, Columbia University, New York, New York; Nathan Kline Institute, Orangeburg, New York. Electronic address: joshua.kantrowitz@nyspi.columbia.edu.

Funding

D-serine augmentation of neuroplasticity-based auditory learning in schizophreniaR33MH116093 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI KANTROWITZ, JOSHUA TOLKIEN · 2021 to 2023
$1.4M
D-serine augmentation of neuroplasticity-based auditory learning in schizophreniaR61MH116093 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI KANTROWITZ, JOSHUA TOLKIEN · 2019 to 2020
$1.2M
NIMH NIH HHS R33 MH116093NIMH NIH HHS R61 MH116093
6 · The paper itself

Abstract

Cognitive impairment associated with schizophrenia (CIAS) and related deficits in learning (plasticity) are among the leading causes of disability in schizophrenia. Despite this, there are no Food and Drug Administration-approved treatments for CIAS, and the development of treatments has been limited by numerous phase 2/3 failures of compounds that showed initial promise in small-scale studies. NMDA-type glutamate receptors (NMDARs) have been proposed to play an important role in schizophrenia; moreover, the NMDAR has a well-characterized role in cognition, learning, and neuroplasticity. We review previously published clinical trials in CIAS that focused on NMDAR modulator treatments, focusing on published and recent developments of the use of novel NMDAR-modulating treatments for CIAS both alone and combined with plasticity/learning paradigms to enhance learning. We use this discussion of previous studies to highlight the importance of incorporating pharmacodynamic target engagement biomarkers early in treatment development, which can help predict which compounds will succeed or fail in phase 3. A range of direct and indirect NMDAR modulators are covered, including D-serine, D-cycloserine, memantine, and glycine and first-generation glycine transport inhibitors (e.g., sarcosine and bitopertin), as well as recent positive studies of iclepertin, a novel glycine transport inhibitor, and luvadaxistat, a D-amino acid oxidase inhibitor that increases brain D-serine levels, and indirect noninvasive brain stimulation NMDAR-modulating treatments. Several examples of successful use of pharmacodynamic target engagement biomarkers for dose/drug discovery are emphasized, including the mismatch negativity, auditory steady state, and time-frequency event-related potential approaches.

Indexed as

Neuronal PlasticityReceptors, N-Methyl-D-AspartateSchizophreniaAnimalsAntipsychotic AgentsHumansAntipsychotic AgentsReceptors, N-Methyl-D-AspartateClinical trialCognitive impairment associated with schizophrenia (CIAS)Mismatch negativityNMDA receptorPlasticityTarget engagement

Identifiers

PMID39218136
PMCPMC11634630

What OpenQuestion holds

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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.