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Online ISSN: 1096-8628    Print ISSN: 0148-7299
American Journal of Medical Genetics

Articles Available Online in Advance of Print
American Journal of Medical Genetics Part A
Published Online: 16 Jan 2003

Copyright © 2003 Wiley-Liss, Inc.

Rapid Publication
 

Sudden infant death syndrome: Association with a promoter polymorphism of the serotonin transporter gene
Debra E. Weese-Mayer 1 *, Elizabeth M. Berry-Kravis 1, Brion S. Maher 2, Jean M. Silvestri 1, Mark E. Curran 3, Mary L. Marazita 2 4
1Department of Pediatrics, Rush Children's Hospital at Rush-Presbyterian-St. Luke's Medical Center, Rush University, Chicago, Illinois
2Center for Craniofacial and Dental Genetics, Division of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
3DNA Sciences, Inc., Fremont, California
4Department of Human Genetics, Graduate School of Public Health, and Department of Oral and Maxillofacial Surgery, School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
 
email: Debra E. Weese-Mayer (dweese@rush.edu)

*Correspondence to Debra E. Weese-Mayer, Professor of Pediatrics at Rush University, Director, Pediatric Respiratory Medicine at Rush Children's Hospital, 1653 West Congress Parkway, Chicago, IL 60612.

Funded by:
 C.J. Foundation for SIDS
 The Sara Lee Foundation
 The Justin Carl Suth SIDS Research Fund
 The Joseph Tyler Gertler SIDS Research Fund
 The University of Maryland Brain Bank and Tissue Bank for Developmental Disorders http://medschool.umaryland.edu/btbank/main.html

Keywords
sudden infant death syndrome • 5HTT • serotonin transporter
Abstract
Serotonergic receptor binding in the arcuate nucleus, n. raphé obscurus, and other medullary regions is decreased in sudden infant death syndrome (SIDS) cases. Further, a variable tandem repeat sequence polymorphism in the promoter region of the serotonin transporter protein (5-HTT) gene has recently been associated with risk of SIDS in a Japanese cohort. This polymorphism differentially regulates 5-HTT expression, with the long allele (L), the SIDS-associated allele, being a more effective promoter than the short allele (S). We therefore investigated the 5-HTT promoter polymorphism in a cohort of 87 SIDS cases (43 African American and 44 Caucasian) and gender/ethnicity-matched controls. Significant positive associations were found between SIDS and the 5-HTT genotype distribution (P = 0.022), specifically with the L/L genotype (P = 0.048), and between SIDS and the 5-HTT L allele (P = 0.005). There was also a significant negative association between SIDS and the S/S genotype (P = 0.011). The comparisons were repeated in the African American and Caucasian subgroups. The data patterns were consistent in the subgroups, i.e., the L/L genotype and L allele were increased in the cases, but not all subgroup comparisons were statistically significant. These results indicate a relationship between SIDS and the L allele of the 5-HTT gene in African Americans and Caucasians, and if confirmed, will provide an important tool for identifying at-risk individuals and estimating the risk of recurrence. © 2003 Wiley-Liss, Inc.

Received: 8 November 2002; Accepted: 11 December 2002

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