Evidence map›Paper›PMID 24321711›Full record

ArticleSchizophrenia research2014

White matter abnormalities in 22q11.2 deletion syndrome: preliminary associations with the Nogo-66 receptor gene and symptoms of psychosis.

Matthew D Perlstein, Moeed R Chohan, Ioana L Coman, Kevin M Antshel, Wanda P Fremont, Matthew H Gnirke, Zora Kikinis, Frank A Middleton, Petya D Radoeva, Martha E Shenton and 1 more

Open access · greenAbstract read
In one paragraph

Article in Schizophrenia research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  13. White matter pathways and social cognition.Neuroscience and biobehavioral reviews · 2018
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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

11 authors at 2 institutions in 1 country.

Matthew D PerlsteinDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Moeed R ChohanDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Ioana L ComanDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Kevin M AntshelDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States; Department of Psychology, Syracuse University, Syracuse, NY, United States.
Wanda P FremontDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Matthew H GnirkeDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Zora KikinisDepartment of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Frank A MiddletonDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States; Department of Neuroscience and Physiology, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Petya D RadoevaDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States.
Martha E ShentonDepartment of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States; Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States; Clinical Neuroscience Division, Laboratory of Neuroscience, Department of Psychiatry, VA Boston Healthcare System, Harvard Medical School, Boston, MA, United States.
Wendy R KatesDepartment of Psychiatry and Behavioral Sciences, State University of New York at Upstate Medical University, Syracuse, NY, United States. Electronic address: katesw@upstate.edu.
SUNY Upstate Medical University · USBrigham and Women's Hospital · US

Funding

Biomarkers for Psychosis in Velocardiofacial SyndromeR01MH064824 · NIMH · UPSTATE MEDICAL UNIVERSITY · PI KATES, WENDY · 2002 to 2015
$7.3M
NIMH NIH HHS MH064824NIMH NIH HHS R01 MH064824
6 · The paper itself

Abstract

backgroundThis study utilized diffusion tensor imaging (DTI) to analyze white matter tractography in the anterior limb of the internal capsule (ALIC), fornix, and uncinate fasciculus (UF) of individuals with 22q11.2 deletion syndrome and controls. Aberrations in these tracts have been previously associated with schizophrenia. With up to 25% of individuals with 22q11.2DS developing schizophrenia in adulthood, we hypothesized reduction in structural integrity of these tracts, including an association with prodromal symptoms of psychosis. We further predicted an association between allelic variation in a functional polymorphism of the Nogo-66 receptor gene and 22q11.2DS white matter integrity.

methodsTractography was conducted using fiber assignment by streamline tracking algorithm in DTI Studio. Subjects were genotyped for the rs701428 SNP of the Nogo-66 receptor gene, and assessed for presence of prodromal symptoms.

resultsWe found significant group differences between 22q11.2DS and controls in DTI metrics for all three tracts. DTI metrics of ALIC and UF were associated with prodromal symptoms in 22q11.2DS. Further, ALIC DTI metrics were associated with allelic variation of the rs701428 SNP of the Nogo-66 receptor gene in 22q11.2DS.

conclusionsAlterations in DTI metrics suggest white matter microstructural anomalies of the ALIC, fornix, and UF in 22q11.2DS. Structural differences in ALIC appear to be associated with the Nogo-66 receptor gene, which has been linked to myelin-mediated axonal growth inhibition. Moreover, the association between psychosis symptoms and ALIC and UF metrics suggests that the Nogo-66 receptor gene may represent a susceptibility gene for psychosis through its disruption of white matter microstructure and myelin-associated axonal growth.

Indexed as

AdolescentCerebral CortexDiffusion Tensor ImagingDiGeorge SyndromeFemaleGene FrequencyGenetic Association StudiesGenetic TestingGenotypeGPI-Linked ProteinsHumansLeukoencephalopathiesMaleMultivariate AnalysisMyelin ProteinsNeuropsychological TestsGPI-Linked ProteinsMyelin ProteinsNogo Receptor 1Receptors, Cell SurfaceRTN4R protein, humanAnterior limb of internal capsuleDiffusion tensor imaging (DTI)rs701428RTN4R geneUncinate fasciculusVelo-cardio-facial syndrome

Identifiers

PMID24321711
PMCPMC3909835
OpenAlexW2123220482

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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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.