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Transmission disequilibrium tests confirm the link between DRD4 gene polymorphism and infant attachment
Author(s) -
Gervai Judit,
Nemoda Zsofia,
Lakatos Krisztina,
Ronai Zsolt,
Toth Ildiko,
Ney Krisztina,
SasvariSzekely Maria
Publication year - 2004
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30102
Subject(s) - transmission disequilibrium test , haplotype , allele , genetics , exon , linkage disequilibrium , biology , disequilibrium , polymorphism (computer science) , gene , medicine , ophthalmology
Abstract Following up the results of a previous population association study (Lakatos et al. [2000: Mol Psychiatry 5:633–637; Lakatos et al. [2002: Mol Psychiatry 7:27–31]) by analyses based on parental genetic data confirmed the link between infant attachment and the dopamine D4 receptor ( DRD4 ) gene. Extended transmission disequilibrium tests (ETDT) were performed to determine whether biased transmission of exon III 48 basepair repeat alleles occurred to infants displaying disorganized and secure attachment behavior with their mothers. The overall allele‐wise TDTs were significant for both groups ( P = 0.038 and 0.020, respectively): a trend for preferential transmission of the seven‐repeat allele to disorganized infants was observed (TDT χ 2 = 3.27, df = 1, P = 0.071), and there was a significant non‐transmission of the same allele to securely attached infants (TDT χ 2 = 6.00, df = 1, P = 0.014). Analysis of haplotypes of the exon III repeat and the −521 C/T promoter polymorphisms in family trios showed that the transmission bias in the larger secure group was due to the low‐rate transmission of the T.7 haplotype containing both the seven‐repeat and the −521 T alleles (TDT χ 2 = 4.46, df = 1, P = 0.035). This suggests that not carrying the T.7 haplotype of the DRD4 gene may act as a resilience factor in the optimal development of early attachment. © 2004 Wiley‐Liss, Inc.