Genetics
Research data support the familial transmission of
ADHD and CD and suggest that these disorders may share common famil-ial
vulnerabilities (Biederman et al.,
1992). Estimates of heritability range from 60 to 80% for ADHD (Sherman et al., 1997) and from 30 to 70% for CD
(Slutske et al., 1997).
Newer molecular genetic studies have identified a
number of individual genes as potential candidate genes in the AD-DBDs.
Evidence of altered DA activity in ADHD has focused on the search for candidate
genes among DA system genes, including the DA D2, DA D4 and DA D5 receptor
genes and the DA trans-porter gene (DAT1; with the strongest evidence for the
7-repeat allele of DRD4 (Swanson et al.,
1998), which mediates a blunted intracellular response to DA, and the 10-repeat
allele of DAT1 (Daly et al., 1999),
which is linked to elevated DA reuptake. Preliminary data have also linked the
10-repeat allele of DAT1 with poor response to methylphenidate (Winsberg and
Comings, 1999), which acts primarily by inhibiting the DA transporter in the
striatum.
Several 5-HT system genes have been identified as
candi-dates for study in CD. These include the genes encoding the en-zymes
tryptophan hydroxylase (TPH)) and monoamine oxidase A (MAOA), which are
involved in the synthesis and metabolism of 5-HT, respectively.
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