Abstract
Antisocial personality disorder (ASPD) is a pervasive condition among youngsters around the globe, which has particular pungency in countries where the socioeconomic context favors delinquency. Several behavioral genetics studies have linked the disorder to the presence of copies of a polymorphic variation of the MAO-A gene that leads to enzymatic hypofunction. An emerging tendency in this literature is to also associate it to the presence of short variations of the 5- HTTLPR polymorphism, which is well-known for its possible role in the vulnerability to major depression of individuals that were exposed to early-life stress. The current paper argues that the association of these findings introduces a theoretical problem that is not trivial (“an apparent paradox”), and further proposes a solution to it.
Keywords: Antisocial Personality Disorder, Etiology, Behavioral Genetics, Major Depression, Endophenotypes, Antisocial, Hyperactivation, neurobiological, polymorphisms, ASPD
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