Page 100 - Like me, or else... - Michelle Achterberg

Chapter 4
All other ROIs showed no behavioral-brain associations (all p’s>.05, see Table 4). Results did not change after exclusion of children with an Axis-I disorder (Table S4). Note that we did not observe any significant clusters of activation scaling with behavior when we performed exploratory whole brain regression analyses with the consecutive noise blast difference scores as covariates of interest (on the contrasts positive>negative, negative>positive, positive>neutral and negative>neutral).
Twin analyses
To investigate twin-effects we calculated Pearson’s correlations for neural activation during social feedback in the 10 ROIs for MZ (n=87) and DZ (n=71) twins, see Table 5. Behavioral genetic analyses revealed that only variance in activation in regions following positive feedback was influenced by genetic factors. Specifically, genetics accounted for 13% (95% CI: 0-32%) of the variance in left DLPFC activation and for 14% (95% CI: 0 - 34%) of the variance in right DLPFC (Table 5). Ten percent of the variance in SMA (95% CI: 0-31%) and right caudate (95% CI: 0-29%) activation was explained by genetics (see Table 5). Estimates for the shared environment were zero, and all of the residuary variance was explained by E (unique environment and measurement error). Genetic modeling for neural activation in the other ROIs revealed minimal or no influence of either genetics or shared environment (estimates 0-4%), and were best explained by unique environment and/or measurement error (Table 5). Variance in neural activation in all ROIs was best explained by an E-model (Table S2).
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