Linked Life Data

21420833

Source:http://linkedlifedata.com/resource/pubmed/id/21420833

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2011-5-2
pubmed:abstractText
Marijuana exposure during the critical period of adolescent brain maturation may disrupt neuro-modulatory influences of endocannabinoids and increase schizophrenia susceptibility. Cannabinoid receptor 1 (CB1/CNR1) is the principal brain receptor mediating marijuana effects. No study to-date has systematically investigated the impact of CNR1 on quantitative phenotypic features in schizophrenia and inter-relationships with marijuana misuse. We genotyped 235 schizophrenia patients using 12 tag single nucleotide polymorphisms (tSNPs) that account for most of CB1 coding region genetic variability. Patients underwent a high-resolution anatomic brain magnetic resonance scan and cognitive assessment. Almost a quarter of the sample met DSM marijuana abuse (14%) or dependence (8%) criteria. Effects of CNR1 tSNPs and marijuana abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co-morbid alcohol/non-marijuana illicit drug misuse as covariates. Significant main effects of CNR1 tSNPs (rs7766029, rs12720071, and rs9450898) were found in white matter (WM) volumes. Patients with marijuana abuse/dependence had smaller fronto-temporal WM volumes than patients without heavy marijuana use. More interestingly, there were significant rs12720071 genotype-by-marijuana use interaction effects on WM volumes and neurocognitive impairment; suggestive of gene-environment interactions for conferring phenotypic abnormalities in schizophrenia. In this comprehensive evaluation of genetic variants distributed across the CB1 locus, CNR1 genetic polymorphisms were associated with WM brain volume variation among schizophrenia patients. Our findings suggest that heavy cannabis use in the context of specific CNR1 genotypes may contribute to greater WM volume deficits and cognitive impairment, which could in turn increase schizophrenia risk.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1573-2509
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
66-75
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:21420833-Adolescent, pubmed-meshheading:21420833-Adult, pubmed-meshheading:21420833-Brain, pubmed-meshheading:21420833-Cognition Disorders, pubmed-meshheading:21420833-Female, pubmed-meshheading:21420833-Follow-Up Studies, pubmed-meshheading:21420833-Genetic Predisposition to Disease, pubmed-meshheading:21420833-Genotype, pubmed-meshheading:21420833-Humans, pubmed-meshheading:21420833-Linkage Disequilibrium, pubmed-meshheading:21420833-Magnetic Resonance Imaging, pubmed-meshheading:21420833-Male, pubmed-meshheading:21420833-Marijuana Abuse, pubmed-meshheading:21420833-Nerve Fibers, Myelinated, pubmed-meshheading:21420833-Neuropsychological Tests, pubmed-meshheading:21420833-Polymorphism, Single Nucleotide, pubmed-meshheading:21420833-Receptor, Cannabinoid, CB1, pubmed-meshheading:21420833-Schizophrenia, pubmed-meshheading:21420833-Young Adult
pubmed:year
2011
pubmed:articleTitle
Cannabinoid receptor 1 gene polymorphisms and marijuana misuse interactions on white matter and cognitive deficits in schizophrenia.
pubmed:affiliation
Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA 5224, USA. beng-ho@uiowa.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural