Evidence map›Paper›PMID 29169997›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2018

PSD95: A synaptic protein implicated in schizophrenia or autism?

Austin A Coley, Wen-Jun Gao

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed, 6 pooled it
7.9field-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

169 citing papers in PubMed, 6 syntheses or guidelines pooled it, 357 citations in OpenAlex.

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  7. PSD-95 drives binocular vision maturation critical for predation.bioRxiv : the preprint server for biology · 2026
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109 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.

Austin A ColeyDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA 19129, United States.
Wen-Jun GaoDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA 19129, United States. Electronic address: wg38@drexel.edu.
Drexel University · US

Funding

Development of NMDAR hypofunction and cognitive deficitsR01MH085666 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2009 to 2018
$3.8M
PSD-95 deficiency alters glutamatergic synapses during development in the prefrontal cortexK00MH124182 · NIMH · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI COLEY, AUSTIN · 2020 to 2023
$274k
PSD-95 deficiency alters glutamatergic synapses during development in the prefrontal cortexF99NS105185 · NINDS · DREXEL UNIVERSITY · PI COLEY, AUSTIN · 2017 to 2018
$89k
NIMH NIH HHS K00 MH124182NIMH NIH HHS R01 MH085666NINDS NIH HHS F99 NS105185
6 · The paper itself

Abstract

The molecular components of the postsynaptic density (PSD) in excitatory synapses of the brain are currently being investigated as one of the major etiologies of neurodevelopmental disorders such as schizophrenia (SCZ) and autism. Postsynaptic density protein-95 (PSD-95) is a major regulator of synaptic maturation by interacting, stabilizing and trafficking N-methyl-d-aspartic acid receptors (NMDARs) and α-amino-3-hydroxy-5-methyl-4-isox-azoleproprionic acid receptors (AMPARs) to the postsynaptic membrane. Recently, there has been overwhelming evidence that associates PSD-95 disruption with cognitive and learning deficits observed in SCZ and autism. For instance, recent genomic and sequencing studies of psychiatric patients highlight the aberrations at the PSD of glutamatergic synapses that include PSD-95 dysfunction. In animal studies, PSD-95 deficiency shows alterations in NMDA and AMPA-receptor composition and function in specific brain regions that may contribute to phenotypes observed in neuropsychiatric pathologies. In this review, we describe the role of PSD-95 as an essential scaffolding protein during synaptogenesis and neurodevelopment. More specifically, we discuss its interactions with NMDA receptor subunits that potentially affect glutamate transmission, and the formation of silent synapses during critical time points of neurodevelopment. Furthermore, we describe how PSD-95 may alter dendritic spine morphologies, thus regulating synaptic function that influences behavioral phenotypes in SCZ versus autism. Understanding the role of PSD-95 in the neuropathologies of SCZ and autism will give an insight of the cellular and molecular attributes in the disorders, thus providing treatment options in patients affected.

Indexed as

AnimalsAutism Spectrum DisorderDisks Large Homolog 4 ProteinHumansSchizophreniaSynapsesDisks Large Homolog 4 ProteinAMPARAutismGlutamateNeurodevelopmentNMDARPSD-95Schizophrenia

Identifiers

PMID29169997
PMCPMC5801047
OpenAlexW2770631390

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.