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A case-control and family-based association study of the 5-HTTLPR in pediatric-onset depressive disorders
Maria Nobile1, Maria Giulia Cataldo, Roberto Giorda
1Child Psychiatry Unit, Eugenio Medea Scientific Institute, Bosisio, Parini, Italy. mnobile@bp.lnf.it
Insights
The serotonin transporter gene promoter polymorphism (5-HTTLPR) SS-genotype and S-allele are linked to childhood depressive disorders (DD). This suggests a potential genetic role for 5-HTTLPR in pediatric depression, requiring further research.
Area of Science:
- Genetics
- Psychiatry
- Molecular Biology
Background:
- Pediatric depression offers insights into mood disorder etiology.
- Understanding genetic factors in early-onset depression is crucial.
Purpose of the Study:
- To investigate the association between the serotonin transporter-linked promoter polymorphism (5-HTTLPR) and childhood- and early-adolescent-onset depressive disorders (DD).
Main Methods:
- A case-control study included 68 patients with DD and 68 matched healthy controls.
- A family-based study involved 41 triads and 11 dyads.
Main Results:
- An excess of the SS-genotype and S-allele was observed in children with DD.
- Family studies indicated preferential transmission of the S-allele to depressed children.
Conclusions:
- The 5-HTTLPR locus is suggested to play a role in childhood DD.
- Replication in larger cohorts is needed to confirm these findings.
Background:
Pediatric depression can be particularly informative for clarification of the causes of mood disorders. The aim of this work was to explore the possible association between childhood- and early-adolescent-onset DSM-IV depressive disorders (DD; including major depression and dysthymia) and the serotonin transporter-linked promoter polymorphism (5-HTTLPR) locus.
Methods:
The case-control sample consisted of 68 unrelated patients with DD, and 68 unrelated age- and gender-matched healthy control subjects. The same patients were included in the family-based study, which consisted of 41 triads and 11 dyads.
Results:
An excess of the SS-genotype (p =.025) and of the S-allele (p =.021) was found among DD children (odds ratio = 1.81; 95% confidence interval = 1.12-2.94). The family-based results suggested that the S-allele was preferentially transmitted to depressed children (haplotype-based haplotype relative risk: chi(2) = 7.231 df = 1, p =.007; transmission disequilibrium test: chi(2) = 5.233, df = 1, p =.022).
Conclusions:
A role for the 5-HTTLPR locus that needs replication in larger samples is suggested in childhood DD.
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