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Vol. 57, No. 2, 2004
Issue release date: June 2004
Section title: Original Paper
Hum Hered 2004;57:59–68
(DOI:10.1159/000077543)

A Novel Permutation Testing Method Implicates Sixteen Nicotinic Acetylcholine Receptor Genes as Risk Factors for Smoking in Schizophrenia Families

Faraone S.V. · Su J. · Taylor L. · Wilcox M. · van Eerdewegh P. · Tsuang M.T.
aHarvard Medical School Department of Psychiatry at the Massachusetts General Hospital, bDepartment of Epidemiology, Harvard School of Public Health, cHarvard Medical School Department of Psychiatry at the Massachusetts Mental Health Center, Boston, Mass., dGenome Therapeutics Corporation, Waltham, Mass., and eDepartment of Psychiatry, University of California, San Diego, Calif., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 6/15/2004

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 4

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: http://www.karger.com/HHE

Abstract

Smoking is a common correlate of schizophrenia, which leads to medical morbidity. Although twin and adoption studies have consistently implicated genes in the etiology of both smoking and schizophrenia, finding genes has been difficult. Several authors have suggested that clinical or neurobiological features associated with schizophrenia, such as smoking, might improve the ability to detect schizophrenia susceptibility genes by identifying genes related to the etiology of that feature. The objective of this study is to assess evidence for linkage of sixteen nicotinic acetylcholine receptor genes and smoking in schizophrenia families, using data from the NIMH Genetics Initiative for schizophrenia. Sixteen nicotinic acetylcholine receptor genes were selected prior to analysis. We used a multipoint sibling pair linkage analysis program, SIBPAL2, with a smoking trait in schizophrenia families. The significance of the group of candidate genes, in addition to each individual candidate gene, was assessed using permutation testing, which adjusted for multiple comparisons. The group of genes showed significant linkage to the smoking trait after adjusting for multiple comparisons through permutation testing (p = 0.039). In addition, two of the individual candidate genes were significant (CHRNA2, p = 0.044) and (CHRNB2, p = 0.015) and two genes were marginally significant (CHRNA7, p = 0.095; CHRNA1, p = 0.076). The significance of the complex hypothesis, involving sixteen genes, implicates the nicotinic system in smoking for schizophrenic families. Individual gene analysis suggests that CHRNA2 and CHRNB2 may play a particular role in this involvement. Such findings help prioritize genes for future case control studies. In addition, we provide a novel permutation method that is useful in future analyses involving a single hypothesis, with multiple candidate genes.


  

Author Contacts

Stephen V. Faraone, PhD
Harvard Medical School
Department of Psychiatry at the Massachusetts General Hospital
37 Shields Ave, Brockton, MA 02301 (USA)
Tel. +1 508 584 6354, Fax +1 508 584 1023, E-Mail sfaraone@hms.harvard.edu

  

Article Information

Received: August 18, 2002
Accepted after revision: December 29, 2003
Number of Print Pages : 10
Number of Figures : 0, Number of Tables : 4, Number of References : 88

  

Publication Details

Human Heredity (International Journal of Human and Medical Genetics)
Founded 1950 as Acta Genetica et Statistica Medica by Gunnar Dahlberg; Continued by M. Hauge (1965–1983)

Vol. 57, No. 2, Year 2004 (Cover Date: Released June 2004)

Journal Editor: J. Ott, New York, N.Y.
ISSN: 0001–5652 (print), 1423–0062 (Online)

For additional information: http://www.karger.ch/journals/hhe


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 6/15/2004

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 4

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: http://www.karger.com/HHE


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