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Misconceptions, Experimental Design, and Behavioral Genetics
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
The relationship between genetics and aggression is often misconceived. The XYY chromosome episode was highly publicized, and media and even early researchers led the public to believe in a “super-male” who was highly dangerous.
Early-life adversity-induced long-term epigenetic programming associated with early onset of chronic physical aggression: Studies in humans and animals
Published in The World Journal of Biological Psychiatry, 2019
Dimitry A. Chistiakov, Vladimir P. Chekhonin
As mentioned above, genetic factors determine up to half of the incidence of physical aggression in humans (Brendgen et al. 2006; Tuvblad et al. 2009). In fact, data on the genetic impact on aggressive behaviour obtained from genetic association studies are limited by several polymorphisms of genes involved in the metabolism and function of serotonergic and dopaminergic circuits. The genetics of aggression has been reviewed in several recent papers (Waltes et al. 2016; Veroude et al. 2016). Low cerebrospinal fluid (CSF) levels of serotonin (5-HT) and its terminal metabolite 5-hydroxyindolacetic acid (5-HIAA) correlate with a higher rate of aggression in humans (Pavlov et al. 2012; Glick 2015) and macaques (Higley et al. 1996; Westergaard et al. 1999). Compared with wild-type peers, mice deficient for the serotonin receptor 5-HT1B seem to be more aggressive since they attacked intruders more frequently and rapidly (Saudou et al. 1994; Ramboz et al. 1996). In mutant mice, the deficiency of receptor-induced hyperlocomotor activity was shown by administration of the 5-HT1A/1B agonist RU24969 (Saudou et al. 1994). However, systemic injections of anti-aggressive doses of certain 5-HT(1A) and (1B) agonists were observed to robustly reduce aggression without loss of motor activity (de Boer & Koolhaas 2005). The differential role of the 5-HT1A receptor was then shown in aggressive and non-aggressive mouse strains. Of the aggressive tested strains, two of three of them had increased 5-HT1A (auto) receptor sensitivity and reduced levels of serotonin in the prefrontal cortex, thereby suggesting the validity of the serotonin-deficiency hypothesis of aggression (Caramaschi et al. 2007).