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No Genetic Linkage Detected for Schizophrenia to Xq27–q28

Published online by Cambridge University Press:  02 January 2018

Lynn E. Delisi ,
Timothy J. Crow ,
Kay E. Davies ,
Joseph D. Terwilliger ,
Jurg Ott ,
Ragnatham Ram ,
Tracey Flint  and
Angela Boccio
Lynn E. Delisi
Affiliation:
Department of Psychiatry, Health Sciences Center, SUNY Stony Brook, Stony Brook, New York 11794, USA
Timothy J. Crow
Affiliation:
Division of Psychiatry, Clinical Research Centre, Northwick Park Hospital, Harrow, Middlesex HA1 3UJ
Kay E. Davies
Affiliation:
Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU
Joseph D. Terwilliger
Affiliation:
Department of Psychiatry and Department of Genetics and Development, Columbia University, New York, USA
Jurg Ott
Affiliation:
Department of Psychiatry and Department of Genetics and Development, Columbia University, New York, USA
Ragnatham Ram
Affiliation:
Department of Psychiatry, SUNY Stony Brook, New York
Tracey Flint
Affiliation:
Institute of Molecular Medicine, University of Oxford
Angela Boccio
Affiliation:
Department of Psychiatry, SUNY Stony Brook, New York
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Abstract

The hypothesis that at least a subgroup of familial cases of schizophrenia could be due to a genetic defect on the X chromosome is supported by the observation of an excess of X-chromosome aneuploidies (XXX and XXY) among populations of patients with psychosis. The distal long arm, Xq27–q28, is a candidate region where linkage has been claimed to manic-depressive disorder and a fragile site has been associated with schizophrenia spectrum disorders. The present study excluded linkage to a large part of this region using four polymorphic probes and multipoint lod-score analysis in 10 families with multiple members with schizophrenia.

Type
Research Article
Information
The British Journal of Psychiatry , Volume 158 , Issue 5 , May 1991 , pp. 630 - 634
Copyright
Copyright © Royal College of Psychiatrists, 1991 

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