Page 88 - Like me, or else... - Michelle Achterberg

Chapter 4
also present in middle childhood, but less pronounced (Achterberg et al., 2017). However, prior studies in children used relatively small samples, which might have been underpowered, specifically since neuroimaging data in developmental samples are more prone to data loss and artifacts due to movement (O'Shaughnessy et al., 2008). The current study therefore set out to include over 500 participants, thereby asserting sufficient sample size and statistical power, even after data loss due to excessive motion (Euser et al., 2016).
Prior studies in adults showed that the DLPFC was negatively related to aggression following social evaluation, suggesting that this region is important for regulating aggression (Achterberg et al. (2016b), see also Riva et al. (2015)). Since the PFC gradually develops until early adulthood (Lenroot and Giedd, 2006; van Duijvenvoorde et al., 2016a), there is ample opportunity for environmental influences. An important question therefore concerns to what extent behavioral and neural responses to social feedback, and subsequent aggression, are influenced by genetic and/or shared environmental factors. Twin models have been particularly important in unraveling to what extent genetic and environmental factors account for the variance in aggression. These studies have shown that trait aggression has both genetic and environmental components (Porsch et al., 2016). Heritability estimates for behavioral aggression are high for both children and adults, explaining up to 48% of the variance (for meta-analyses, see Rhee and Waldman (2002); Ferguson (2010); Tuvblad and Baker (2011)). We aimed to explore whether neural reactions to social feedback that could elicit aggression show similar heritability estimates. Studies of the genetics of functional neuroimaging are currently limited to studies using resting state fMRI (Richmond et al., 2016) or cognitive working memory tasks (Jansen et al., 2015). These studies mostly point to (moderate) genetic influences, with few studies showing significant shared environmental components. It should be noted that these findings are largely based on adult twin studies, whereas previous research showed that heritability estimates of brain measures are stronger in adulthood than in childhood (Lenroot et al., 2009; Lenroot and Giedd, 2011; van den Heuvel et al., 2013). In this study we therefore used a large developmental twin sample (N=509 7-9-year-olds), to investigate i) the heritability of behavioral aggression following social evaluation; ii) the neural underpinnings of social evaluation and their relation to behavioral aggression; and iii) the heritability of these neural underpinnings.
We hypothesized that negative social feedback would result in behavioral aggression (Chester et al., 2014; Achterberg et al., 2016b; Achterberg et al., 2017). Prior studies have shown that trait aggression has a relatively strong genetic component (Porsch et al., 2016), however the influences of genetics and environment on state aggression such as measured with the SNAT are not yet known. On a neural level, we predicted to find a network of regions that process social feedback irrespective of valence, as prior research showed in adults (Achterberg et al., 2016b), including the ACCg and the (anterior) insula. In
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