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A large gap exists between behavior genetics and cognitive neuroscience, although psychologists feature prominently in both fields. Behavior genetics focuses on individual differences and, through sophisticated statistical modeling in twin and family studies, addresses the genetic and environmental contribution to variation in cognitive ability. Cognitive neuroscience tends to focus on species universals in brain function during specific cognitive operations, which are isolated by clever experimental design, and located in the time and (brain) space by modern imaging techniques. This paper describes the complementary approach of "genetic neuroscience" that integrates the study of cognition as an individual trait and the study of cognition as an universal process. It is argued that the intermediate phenotypes or "endophenotypes" of brain function and structure from neuroscience will boost the power of geneticists' association and linkage approaches to find the genes underlying differences in cognitive ability. Neuroscience, in turn, will profit greatly from successfully identified gene functions. Genes can provide insight in the "black box" between molecular events and cognition. They offer many opportunities to lay bare gene by environment interactions in the psychological laboratory. By reviewing some of the main issues in each field and summarizing the mutual advantages of collaboration between geneticists and neuroscientists we hope to mount further support for a complementary approach.

Changes in genetic and environmental influences on electroencephalographic (EEG) and event-related potential (ERP) indices of neural development were studied in two large cohorts of young (N = 418) and adolescent (N = 426) twins. Individual differences in these indices were largely influenced by genetic factors, and throughout development, the stable part of the variance was mainly genetic. Both EEG power (which describes the amount of variability in brain electrical potentials that can be attributed to different frequencies) and long-distance EEG coherence (which is the squared cross-correlation between two EEG signals at different scalp locations and can be regarded as an index for cortico-cortical connectivity) were highly heritable. ERP-P300 latencies and amplitudes were low to moderately heritable. Clear differences between young children and adolescents could be observed in the heritabilities of EEG and ERP indices. The heritabilities of EEG power and EEG coherence were higher in adolescents than in children, whereas the heritabilities of P300 latencies were lower. Both cohorts (young children and adolescents) were measured twice: The children were tested when they were 5 and again at 7 years, the adolescents when they were 16 and again at 18 years. Therefore, within these age ranges a more detailed analysis of age-related changes in heritabilities and in the emergence of new genetic influences could be studied. The heritabilities of EEG powers and P300 amplitudes and latencies did not change much from age 5 to age 7 and from age 16 to 18 years. The heritabilities of a substantial number of connections within the cortex, however, as indexed by EEG coherence, changed significantly from age 5 to age 7, though not from age 16 to 18. The only changes in the heritabilities in adolescents were connections within the prefrontal cortex, which is in agreement with theories of adolescent development. These age-related changes in the heritabilities may reflect a larger impact of maturation on cortico-cortical connectivity in childhood than in adolescence. Evidence was found for qualitative changes in brain electrophysiology in young children: New genetic factors emerged at age 7 for posterior EEG coherences and for P300 latency at some scalp locations. This supports theories of qualitative stage transitions in this age range, as previously suggested using behavioral and EEG data.

AbstractCrime victimization is associated with a more unfavorable health profile. We examined associations of victimization of property, violence, and sexual crime with mental health indices for depression, anxiety, and loneliness and explore their etiology in Dutch twin families. The data were collected from adult twins, their parents, siblings, spouses, and offspring participating in longitudinal survey studies of the Netherlands Twin Register (N = 19,867). First, we tested if there is an association between victimization and loneliness, anxiety, and depression at the population level. Second, discordant twin pairs were identified, where one twin was a crime victim and the cotwin was not. This design allows controlling for confounding by shared environment and genetic factors. Third, a longitudinal comparison was made of pre- and post-victimization data in victims, their family members, and unrelated individuals. At the population level, victimization was associated with increased depression, anxiety, and loneliness, except for property crime, which was not associated with depression and anxiety. The associations were strongest for violent and sexual crimes. Within discordant twin pairs, no significant differences were found between the victimized and non-victimized twins. These results confirm that crime victimization is associated with adverse mental health outcomes and loneliness, with the strength of this association differing per type of crime. There is no strong evidence that the relationship between victimization and mental health or loneliness follows a simple causal model, as the relationship can be partly explained by genetic and shared environmental confounding. These results also suggest that victims of sexual and violent crimes may already experience more mental health problems before victimization than non-victims, and that individuals with more mental health problems and loneliness are at increased risk of becoming a victim.

Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health.Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n= 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), diastolic, and systolic blood pressure (BP).Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P < 0.012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 x 10(-7) < P < 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 x 10(-8) < P < 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels.Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors. Fund: European Union's Horizon 2020 research and innovation programme under grant agreement no. 633595 DynaHEALTH. (c) 2018 The Authors. Published by Elsevier B.V.

Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health. Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n = 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL—C), triglycerides (TG), diastolic, and systolic blood pressure (BP). Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P < 0·012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 × 10−7 < P < 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 × 10−8 < P < 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels. Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors. Fund: European Union's Horizon 2020 research and innovation programme under grant agreement no. 633595 DynaHEALTH.