Evidence map›Paper›PMID 27430010›Full record

ArticleNPJ schizophrenia2016

Molecular evidence of synaptic pathology in the CA1 region in schizophrenia.

Natalie Matosin, Francesca Fernandez-Enright, Jeremy S Lum, Martin Engel, Jessica L Andrews, Nils C Gassen, Klaus V Wagner, Mathias V Schmidt, Kelly A Newell

Open access · goldAbstract read
In one paragraph

Article in NPJ schizophrenia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 5 pooled it
4.4field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 5 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  10. Spatially resolved translational dysregulation inbioRxiv : the preprint server for biology · 2025
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  15. Cathepsin B modulates microglial migration and phagocytosis of amyloid β in Alzheimer's disease through PI3K-Akt signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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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

9 authors at 3 institutions in 2 countries.

Natalie MatosinDepartments of Translational Research in Psychiatry and Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany; Departments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, Australia; Department of Medicine, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
Francesca Fernandez-EnrightDepartments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, Australia; Department of Health Science, School of Science, Australian Catholic University, Brisbane, QLD, Australia.
Jeremy S LumDepartments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong , Wollongong, NSW, Australia.
Martin EngelDepartments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong , Wollongong, NSW, Australia.ORCID 0000-0001-7602-1340
Jessica L AndrewsDepartments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong , Wollongong, NSW, Australia.
Nils C GassenDepartments of Translational Research in Psychiatry and Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry , Munich, Germany.
Klaus V WagnerDepartments of Translational Research in Psychiatry and Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry , Munich, Germany.
Mathias V SchmidtDepartments of Translational Research in Psychiatry and Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry , Munich, Germany.
Kelly A NewellDepartments of Science, Medicine and Health, and Social Sciences, Illawarra Health and Medical Research Institute, University of Wollongong , Wollongong, NSW, Australia.
University of Wollongong · AUMax Planck Institute of Psychiatry · DEIllawarra Health and Medical Research Institute · AU

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
BRAIN TISSUE RESOURCE CENTER FOR ALCOHOL RESEARCHR24AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI KRIL, JILLIAN JUNE · 2000 to 2011
$2.2M
NIAAA NIH HHS R24 AA012725NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

Alterations of postsynaptic density (PSD)95-complex proteins in schizophrenia ostensibly induce deficits in synaptic plasticity, the molecular process underlying cognitive functions. Although some PSD95-complex proteins have been previously examined in the hippocampus in schizophrenia, the status of other equally important molecules is unclear. This is especially true in the cornu ammonis (CA)1 hippocampal subfield, a region that is critically involved in the pathophysiology of the illness. We thus performed a quantitative immunoblot experiment to examine PSD95 and several of its associated proteins in the CA1 region, using post mortem brain samples derived from schizophrenia subjects with age-, sex-, and post mortem interval-matched controls (n=20/group). Our results indicate a substantial reduction in PSD95 protein expression (-61.8%). Further analysis showed additional alterations to the scaffold protein Homer1 (Homer1a: +42.9%, Homer1b/c: -24.6%), with a twofold reduction in the ratio of Homer1b/c:Homer1a isoforms (P=0.011). Metabotropic glutamate receptor 1 (mGluR1) protein levels were significantly reduced (-32.7%), and Preso, a protein that supports interactions between Homer1 or PSD95 with mGluR1, was elevated (+83.3%). Significant reduction in synaptophysin (-27.8%) was also detected, which is a validated marker of synaptic density. These findings support the presence of extensive molecular abnormalities to PSD95 and several of its associated proteins in the CA1 region in schizophrenia, offering a small but significant step toward understanding how proteins in the PSD are altered in the schizophrenia brain, and their relevance to overall hippocampal and cognitive dysfunction in the illness.

Identifiers

PMID27430010
PMCPMC4944906
OpenAlexW2460172330

What OpenQuestion holds

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LicenceCC BY
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.