| Association of schizophrenia in 22q11.2 deletion syndrome and gray matter volumetric deficits in the superior temporal gyrus. | |
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MedLine Citation:
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PMID: 21362743 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Individuals with 22q11.2 deletion syndrome are known to be at high risk of developing schizophrenia. Previous imaging studies have provided limited data on the relation of schizophrenia expression in 22q11.2 deletion syndrome to specific regional brain volumetric changes. The authors hypothesized that the main structural brain finding associated with schizophrenia expression in 22q11.2 deletion syndrome, as for schizophrenia in the general population, would be gray matter volumetric deficits, especially in the temporal lobes. METHOD: MR brain images from 29 patients with 22q11.2 deletion syndrome and schizophrenia and 34 comparison subjects with 22q11.2 deletion syndrome and no history of psychosis were analyzed using a voxel-based morphometry method that also yielded volumes for related region-of-interest analyses. The authors compared data from the two groups using an analysis of covariance model correcting for total intracranial volume, age, sex, IQ, and history of congenital cardiac defects. The false discovery rate threshold was set at 0.05 to account for multiple comparisons. RESULTS: Voxel-based morphometry analyses identified significant gray matter reductions in the left superior temporal gyrus (Brodmann's area 22) in the schizophrenia group. There were no significant between-group differences in white matter or CSF volumes. Region-of-interest analyses showed significant bilateral gray matter volume reductions in the temporal lobes and superior temporal gyri in the schizophrenia group. CONCLUSIONS: The structural brain expression of schizophrenia associated with the highly penetrant 22q11.2 deletion involves lower gray matter volumes in temporal lobe regions. These structural MRI findings in a 22q11.2 deletion syndrome form of schizophrenia are consistent with those from studies involving schizophrenia samples from the general population. The results provide further support for 22q11.2 deletion syndrome as a genetic subtype and as a useful neurodevelopmental model of schizophrenia. |
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Authors:
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Eva W C Chow; Andrew Ho; Corie Wei; Eduard H J Voormolen; Adrian P Crawley; Anne S Bassett |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-03-01 |
Journal Detail:
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Title: The American journal of psychiatry Volume: 168 ISSN: 1535-7228 ISO Abbreviation: Am J Psychiatry Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-03 Completed Date: 2011-06-29 Revised Date: 2012-02-27 |
Medline Journal Info:
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Nlm Unique ID: 0370512 Medline TA: Am J Psychiatry Country: United States |
Other Details:
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Languages: eng Pagination: 522-9 Citation Subset: AIM; IM |
Affiliation:
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Clinical Genetics Research Program, Centre for Addiction and Mental Health, Toronto, Canada. eva.chow@utoronto.ca |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Analysis of Variance Chromosome Deletion* Chromosomes, Human, Pair 22 / genetics* DiGeorge Syndrome / genetics Female Humans Magnetic Resonance Imaging Male Organ Size / genetics Schizophrenia / genetics*, pathology Temporal Lobe / pathology* |
| Grant Support | |
ID/Acronym/Agency:
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107520//Canadian Institutes of Health Research; MOP-74631//Canadian Institutes of Health Research; MOP-79518//Canadian Institutes of Health Research; MOP-89066//Canadian Institutes of Health Research; MOP-97800//Canadian Institutes of Health Research |
| Comments/Corrections | |
Erratum In:
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Am J Psychiatry. 2011 May;168(5):553 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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