Association analysis of 15 polymorphisms within 10 candidate genes for antisocial behavioural traits

Abstract

This study sought to test 15 simple sequence repeat polymorphisms within 10 candidate genes for association with antisocial behavioural traits. Genes included were those known to regulate dopamine synthesis and transmission in the brain (DBH, DRD2, MAOA, TFAP2B, NR4A2, LMX1B) and those involved in the differentiation of social and sexual behaviour in men and women (AR, ESR1, OXTR, AVPR1A). Participants were Caucasians (men=1007, women=1089) aged 20-24 years who were assessed for indicators of antisocial traits such as pseudo-maturity, substance misuse and unstable lifestyle. Significant associations for antisocial traits were found with AR and ESR1 polymorphisms in men, and with polymorphisms within NR4A2 and TFAP2B in women. The association with TFAP2B remained significant after correction for multiple testing. This pattern of associations suggests that genetic variation within transcription factors may in part explain the variation observed in the population for antisocial behavioural phenotypes.

Genetic determinants of aggression and impulsivity in humans

“…These observations were then confirmed by several studies in Europeans and Asians showing a correlation between the carriage of short CAG repeat alleles and antisocial behavior (Prichard et al 2007;Westberg et al 2009), Eysenck's psychoticism (Turakulov et al 2004;Loehlin et al 2005), and aggression (Rajender et al 2008). Furthermore, Aluja et al (in press) showed an implication of both AR repeats in predisposition to impulsive-disinhibited personality traits in Spanish inmates carrying the haplotype comprised of short CAG repeats and long GGC repeats.…”

Behavioral genetics in antisocial spectrum disorders and psychopathy: A review of the recent literature

“…Buckholtz and Meyer-Lindenberg recently reviewed the available literature on MAOA in impulsive aggression, and proposed a mechanism by which the lower activity variants of MAOA could sensitize pertinent neural circuitry to early life stress, while concluding that variation at the MAOA VNTR accounts for only a small amount of variance in risk (Buckholtz & Meyer-Lindenberg, 2008). Not all studies have replicated the findings discussed above (Koller, Bondy, Preuss, Bottlender, & Soyka, 2003;Prichard, Jorm, Mackinnon, & Easteal, 2007;Sjoberg et al, 2007). A few studies suggest that the high activity variants, or longer alleles, may be problematic alone (Tikkanen et al, 2009), under the influence of unfavorable environmental factors (Sjoberg et al, 2007;Vanyukov et al, 2007), or in combination with a delinquent peer group (Beaver & Holtfreter, 2009), while still other studies conclude that the higher activity variants are relatively protective in the face of environmental adversity (e.g.…”

“…The recent work of Rajender and colleagues found that shorter CAG repeats were more common in 374 men who had been convicted of violent criminal offenses as compared with controls matched by ethnicity (Rajender et al, 2008), building on the work of Jonsson and colleagues (Jonsson et al, 2001), which suggested a tendency for shorter CAG repeats to be associated with personality traits related to dominance and aggression on the Karolinska Scale of Personality. The work of Prichard and colleagues in 2007 indicated that highest frequency repeat length in antisocial behavior was seen among men with the medium length repeats, and was not seen among female subjects at all (Prichard et al, 2007). The work of Cheng also did not support the association of short repeats and antisocial behavior (Cheng, Hong, Liao, & Tsai, 2006), and the work of Loehlin suggested that any effects of androgen receptor polymorphisms on personality were weak at best (Loehlin, Jonsson, Gustavsson, Schalling, & Stallings, 2003) and the range of findings in this area appears to bear out this assertion.…”

Discussing the Putative Role of Obesity-Associated Genes in the Etiopathogenesis of Eating Disorders

“…This genotype has been shown to be associated with personality dimensions such as anxiety, psychasthenia, depression or antisocial traits, with the short allele generally correlating with lower scores in the different measured psychological scales [152][153][154][155]. Furthermore, and supporting the aforementioned biological function of TFAP2B, this polymorphism has been suggested to interact with polymorphic sites in the serotonin transporter (5HTTLPR), catechol-O-methyl transferase (COMT ) and monoamino oxidase (MAO)-A genes to modulate additional personality dimensions [154,156].…”