Evidence map›Paper›PMID 21856318›Full record

ReviewNeuropharmacology2012

Extracellular matrix abnormalities in schizophrenia.

Sabina Berretta

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
4.1field-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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.

  1. Pooled it
  2. Article
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  7. Article
  8. Review
  9. Clozapine induces perineuronal net remodeling in a developmental mouse model exhibiting schizophrenia-relevant phenotypes.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
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  13. Review
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  17. Review
  18. Article
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49 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 at 1 institution in 1 country.

Sabina BerrettaTranslational Neuroscience Laboratory, Mclean Hospital, 115 Mill Street, Belmont, MA 02478, USA. s.berretta@mclean.harvard.edu
McLean Hospital · US

Funding

Disruption of Extracellular Matrix-Glial Interactions in SchizophreniaR01MH086522 · NIMH · MCLEAN HOSPITAL · PI BERRETTA, SABINA · 2011 to 2015
$2.0M
Extracellular matrix abnormalities in the medial temporal lobe of subjects with sR21MH083222 · NIMH · MCLEAN HOSPITAL · PI BERRETTA, SABINA · 2008 to 2008
$181k
NIMH NIH HHS R01 MH086522NIMH NIH HHS R21 MH083222
6 · The paper itself

Abstract

Emerging evidence points to the involvement of the brain extracellular matrix (ECM) in the pathophysiology of schizophrenia (SZ). Abnormalities affecting several ECM components, including Reelin and chondroitin sulfate proteoglycans (CSPGs), have been described in subjects with this disease. Solid evidence supports the involvement of Reelin, an ECM glycoprotein involved in corticogenesis, synaptic functions and glutamate NMDA receptor regulation, expressed prevalently in distinct populations of GABAergic neurons, which secrete it into the ECM. Marked changes of Reelin expression in SZ have typically been reported in association with GABA-related abnormalities in subjects with SZ and bipolar disorder. Recent findings from our group point to substantial abnormalities affecting CSPGs, a main ECM component, in the amygdala and entorhinal cortex of subjects with schizophrenia, but not bipolar disorder. Striking increases of glial cells expressing CSPGs were accompanied by reductions of perineuronal nets, CSPG- and Reelin-enriched ECM aggregates enveloping distinct neuronal populations. CSPGs developmental and adult functions, including neuronal migration, axon guidance, synaptic and neurotransmission regulation are highly relevant to the pathophysiology of SZ. Together with reports of anomalies affecting several other ECM components, these findings point to the ECM as a key component of the pathology of SZ. We propose that ECM abnormalities may contribute to several aspects of the pathophysiology of this disease, including disrupted connectivity and neuronal migration, synaptic anomalies and altered GABAergic, glutamatergic and dopaminergic neurotransmission.

Indexed as

AnimalsExtracellular MatrixExtracellular Matrix ProteinsHumansReelin ProteinSchizophreniaSignal TransductionExtracellular Matrix ProteinsReelin ProteinRELN protein, human

Identifiers

PMID21856318
PMCPMC3234338
OpenAlexW2004943408

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.