Literature DB >> 21324950

Maternally derived microduplications at 15q11-q13: implication of imprinted genes in psychotic illness.

Andrés Ingason1, George Kirov, Ina Giegling, Thomas Hansen, Anthony R Isles, Klaus D Jakobsen, Kari T Kristinsson, Louise le Roux, Omar Gustafsson, Nick Craddock, Hans-Jürgen Möller, Andrew McQuillin, Pierandrea Muglia, Sven Cichon, Marcella Rietschel, Roel A Ophoff, Srdjan Djurovic, Ole A Andreassen, Olli P H Pietiläinen, Leena Peltonen, Emma Dempster, David A Collier, David St Clair, Henrik B Rasmussen, Birte Y Glenthøj, Lambertus A Kiemeney, Barbara Franke, Sarah Tosato, Chiara Bonetto, Evald Saemundsen, Stefán J Hreidarsson, Markus M Nöthen, Hugh Gurling, Michael C O'Donovan, Michael J Owen, Engilbert Sigurdsson, Hannes Petursson, Hreinn Stefansson, Dan Rujescu, Kari Stefansson, Thomas Werge.   

Abstract

OBJECTIVE: Rare copy number variants have been implicated in different neurodevelopmental disorders, with the same copy number variants often increasing risk of more than one of these phenotypes. In a discovery sample of 22 schizophrenia patients with an early onset of illness (10-15 years of age), the authors observed in one patient a maternally derived 15q11-q13 duplication overlapping the Prader-Willi/Angelman syndrome critical region. This prompted investigation of the role of 15q11-q13 duplications in psychotic illness.
METHOD: The authors scanned 7,582 patients with schizophrenia or schizoaffective disorder and 41,370 comparison subjects without known psychiatric illness for copy number variants at 15q11-q13 and determined the parental origin of duplications using methylation-sensitive Southern hybridization analysis.
RESULTS: Duplications were found in four case patients and five comparison subjects. All four case patients had maternally derived duplications (0.05%), while only three of the five comparison duplications were maternally derived (0.007%), resulting in a significant excess of maternally derived duplications in case patients (odds ratio=7.3). This excess is compatible with earlier observations that risk for psychosis in people with Prader-Willi syndrome caused by maternal uniparental disomy is much higher than in those caused by deletion of the paternal chromosome.
CONCLUSIONS: These findings suggest that the presence of two maternal copies of a fragment of chromosome 15q11.2-q13.1 that overlaps with the Prader-Willi/Angelman syndrome critical region may be a rare risk factor for schizophrenia and other psychoses. Given that maternal duplications of this region are among the most consistent cytogenetic observations in autism, the findings provide further support for a shared genetic etiology between autism and psychosis.

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Year:  2011        PMID: 21324950      PMCID: PMC3428917          DOI: 10.1176/appi.ajp.2010.09111660

Source DB:  PubMed          Journal:  Am J Psychiatry        ISSN: 0002-953X            Impact factor:   18.112


  39 in total

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