Format

Send to

Choose Destination
See comment in PubMed Commons below
Pediatr Res. 2010 Nov;68(5):409-13. doi: 10.1203/PDR.0b013e3181f2edf0.

Lack of association of the serotonin transporter polymorphism with the sudden infant death syndrome in the San Diego Dataset.

Author information

1
Department of Pathology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA. david.paterson@childrens.harvarvd.edu

Abstract

Dysfunction of medullary serotonin (5-HT)-mediated respiratory and autonomic function is postulated to underlie the pathogenesis of the majority of sudden infant death syndrome (SIDS) cases. Several studies have reported an increased frequency of the LL genotype and L allele of the 5-HT transporter (5-HTT) gene promoter polymorphism (5-HTTLPR), which is associated with increased transcriptional activity and 5-HT transport in vitro, in SIDS cases compared with controls. These findings raise the possibility that this polymorphism contributes to or exacerbates existing medullary 5-HT dysfunction in SIDS. In this study, we tested the hypothesis that the frequency of LL genotype and L allele are higher in 179 SIDS cases compared with 139 controls of multiple ethnicities in the San Diego SIDS Dataset. We observed no significant association of genotype or allele with SIDS cases either in the total cohort or on stratification for ethnicity. These observations do not support previous findings that the L allele and/or LL genotype of the 5-HTTLPR are associated with SIDS.

PMID:
20661167
PMCID:
PMC3242414
DOI:
10.1203/PDR.0b013e3181f2edf0
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for PubMed Central
    Loading ...
    Support Center