Direct analysis of candidate genes in impulsive behaviours.
Antisocial behaviour is both heterogeneous and the product of interacting genetic and environmental factors acting at different levels of causation. Heritability studies show that individual differences in predisposition to antisocial behaviour are transmitted vertically in families by genetic mechanisms. Owing to aetiological heterogeneity and complexity, study of a variety of other behavioural phenotypes may shed more light on the antecedents of antisocial behaviour than direct studies on antisocial behaviour. Identification of genetic vulnerability factors would clarify mechanisms of vulnerability and the role of the environment. Direct gene analysis and genetic linkage analysis have identified structural variants in genes involved in neurotransmitter function, and some progress has been made towards relating these genetic variants to antisocial personality and other behaviours. Thyroid hormone receptor variants can cause attention deficit/hyperactivity disorder, and a monoamine oxidase A variant leads to aggressive behaviour in one family. Direct gene analyses have revealed non-conservative amino acid substitutions and structural variants (generally rare) at DRD2, DRD3 and DRD4 dopamine receptors and 5-HT1A, 5-HT2A, 5-HT2C and 5-HT7 serotonin receptors. The stage is set to identify the phenotypic significance of these as well as genetic variants at other loci which may be relevant as candidate genes for antisocial behaviour and related behavioural differences.
Goldman
D
D
Laboratory of Neurogenetics, NIAAA, NIH, Rockville, MD 20852, USA.
Lappalainen
J
J
Ozaki
N
N
D000818:Animals; D004298:Dopamine / Q000235:genetics; D005544:Forecasting; D005796:Genes; D006801:Humans; D007175:Impulsive Behavior / Q000235:genetics*; D012701:Serotonin / Q000235:genetics
D012701:Serotonin; D004298:Dopamine