C1QTNF7, although none remained significant when individuals were classified dichotomously as cases and controls. Attention-deficit/hyperactivity disorder (ADHD) increases the risk for ASPD,11 and genes that have been previously found in association with ADHD have also been tested for association with ASPD. In a recent study, ADHD linked SNAP25 polymorphisms (DdeI T/T, MnlI T/T haplotype) were associated with novelty-seeking scores in male ASPD subjects, and were more common in ASPD males when compared with sex-matched controls.12 Another candidate gene study revealed an association of COL25A1 variant with comorbid ASPD and substance dependent in a subpopulation of African American and European American samples of substance-dependent patients with ASPD.13 In another recent study, a variant of a previously ADHD linked gene, CDH13, was associated with extreme violent behavior, and replicated in another Finnish cohort of violent offenders.4, 14 In the same study, the MAOA low-activity promoter genotype association with violent criminal behavior was replicated. MAOA deficiency was first reported in association with impulsive and aggressive behavior in a study of a Dutch family cohort,15 and later, MAOA low activity allele and childhood maltreatment interaction was linked to antisocial behavior.16 Recently, Tielbeek et al.17 reported the first genome-wide approach in the analysis of population-based
