Evidence map›Paper›PMID 20691252›Full record

ReviewInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience2011

White matter neuron alterations in schizophrenia and related disorders.

Caroline M Connor, Benjamin C Crawford, Schahram Akbarian

Abstract readReview
In one paragraph

Review in International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Psychosis in Huntington disease: a short update.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  4. Dystrophinopathy with aPCN reports : psychiatry and clinical neurosciences · 2026
    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

3 authors at 2 institutions in 1 country.

Caroline M ConnorBrudnick Neuropsychiatric Research Institute, Department of Psychiatry, University of Massachusetts Medical School, Worcester, MA 01604, USA.
Benjamin C Crawford
Schahram Akbarian
University of Massachusetts Chan Medical School · USNeuropsychiatric Research Institute · US

Funding

Small RNA regulation of BDNF expression in schizophreniaR01MH081943 · NIMH · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AKBARIAN, SCHAHRAM · 2008 to 2012
$1.8M
EPIGENETIC CHANGES IN FRONTAL LOBE OF SCHIZOPHRENICSR01MH071476 · NIMH · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AKBARIAN, SCHAHRAM · 2005 to 2009
$1.7M
NIMH NIH HHS R01 MH071476NIMH NIH HHS R01 MH081943
6 · The paper itself

Abstract

Increased density and altered spatial distribution of subcortical white matter neurons (WMNs) represents one of the more well replicated cellular alterations found in schizophrenia and related disease. In many of the affected cases, the underlying genetic risk architecture for these WMN abnormalities remains unknown. Increased density of neurons immunoreactive for Microtubule-Associated Protein 2 (MAP2) and Neuronal Nuclear Antigen (NeuN) have been reported by independent studies, though there are negative reports as well; additionally, group differences in some of the studies appear to be driven by a small subset of cases. Alterations in markers for inhibitory (GABAergic) neurons have also been described. For example, downregulation of neuropeptide Y (NPY) and nitric oxide synthase (NOS1) in inhibitory WMN positioned at the gray/white matter border, as well as altered spatial distribution, have been reported. While increased density of WMN has been suggested to reflect disturbance of neurodevelopmental processes, including neuronal migration, neurogenesis, and cell death, alternative hypotheses--such as an adaptive response to microglial activation in mature CNS, as has been described in multiple sclerosis--should also be considered. We argue that larger scale studies involving hundreds of postmortem specimens will be necessary in order to clearly establish the subset of subjects affected. Additionally, these larger cohorts could make it feasible to connect the cellular pathology to environmental and genetic factors implicated in schizophrenia, bipolar disorder, and autism. These could include the 22q11 deletion (Velocardiofacial/DiGeorge) syndrome, which in some cases is associated with neuronal ectopias in white matter.

Indexed as

AnimalsBiomarkersBipolar DisorderBrainEndophenotypesHumansNerve Fibers, MyelinatedNeuronsSchizophreniaBiomarkers

Identifiers

PMID20691252
PMCPMC2992083
OpenAlexW2054564838

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.