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The genetic and environmental etiology of individual differences was examined in initial level and change in psychopathic personality from ages 9 to 18 years. A piecewise growth curve model, in which the first change score (G1) influenced all ages (9–10, 11–13, 14–15, and 16–18 years) and the second change score (G2) only influenced ages 14–15 and 16–18 years, fit the data better did than the standard single slope model, suggesting a turning point from childhood to adolescence. The results indicated that variations in levels and both change scores were mainly due to genetic (A) and nonshared environmental (E) influences (i.e., AE structure for G0, G1, and G2). No sex differences were found except on the mean values of level and change scores. Based on caregiver ratings, about 81% of variance in G0, 89% of variance in G1, and 94% of variance in G2 were explained by genetic factors, whereas for youth self-reports, these three proportions were 94%, 71%, and 66%, respectively. The larger contribution of genetic variance and covariance in caregiver ratings than in youth self-reports may suggest that caregivers considered the changes in their children to be more similar as compared to how the children viewed themselves.
The Southern California Twin Register at the University of Southern California (USC) was initiated in 1984 and continues to provide an important resource for studies investigating genetic and environmental influences on human behavior. This article provides an update on the current register and its potential for future twin studies using recruitment through school district databases and voter records. An overview is also provided for an ongoing longitudinal twin study investigating the development of externalizing psychopathology from childhood to young adulthood, the USC Study of Risk Factors for Antisocial Behavior. Characteristics of the twins and their families are presented, including recruitment and participation rates, as well as attrition analyses and a summary of key findings to date.
This chapter reviews how functions of genetic susceptibility factors can be validated, specifically using disrupted in schizophrenia 1 (DISC1) as an example. Studies at multiple levels, from protein chemistry, cell biology, animal study, to clinical work provide comprehensive understanding of the functions of susceptibility factors. Once genetic studies identify candidate susceptibility factors for the diseases, functions of such proteins can be tested in cells by modulating expression of the target molecules or by expressing their genetic variants. The chapter describes rodent models with manipulations for genetic susceptibility factors of mental illnesses in greater detail. A series of studies by Weinberger and associates has pioneered the possible correlation of brain dysfunction with genetic variations in susceptibility factors associated with mental illnesses. To identify mechanistic links from genetic factors to the phenotypes, especially those observed during brain development and maturation, a combination of human studies with animal experiments is expected.