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This chapter reviews the evidence for genetic and environmental influences, both specified and unspecified in antisocial behavior. It discusses heritability of both adult and child mental disorders in DSM-IV-TR, for which antisocial behavior is central to their diagnosis. The chapter also reviews heritability of the related externalizing disorders. It highlights some of the most exciting new directions in this field, which aim to unpack the genetic and environmental black boxes in antisocial behavior, and provides the complexities of the gene-environment interplay in antisocial development. Evidence of genetic influences on antisocial behavior does not implicate that individuals exhibiting antisocial behavior are immune or resistant to interventions. Future research with combined approaches from behavior genetics and neuroscience will lead to better understanding of specific genes that result in structural and functional brain impairments that in turn give rise to antisocial, violent, and psychopathic behavior.
A susceptibility locus for schizophrenia in the pseudoautosomal region has been proposed on the basis of a possible excess of sex chromosome aneuploidies among patients with schizophrenia and an increased sex concordance in affected sib pairs. Several studies investigating this hypothesis have produced conflicting evidence.
In a series of Icelandic and British families, we used lod score and sib pair linkage analyses with markers for the MIC2 and DXYS14 loci on the pseudoautosomal XY region.
Lod and sib pair linkage analysis with these markers produced strongly negative scores. Heterogeneity testing also produced negative results.
We conclude that the present study provides no support for the involvement of either the pseudoautosomal region or the nearby region of the sex chromosomes in the aetiology of schizophrenia.
A multiplex kindred ascertained through a single proband with GTS has been systematically investigated with standardised diagnostic instruments for other cases of GTS and related disorders. Complex segregation analysis supported the hypothesis that a single major gene inherited in autosomal dominant fashion but with incomplete penetrance contributed most of the variance in the liability to develop GTS and related disorders. This result is consistent with previous segregation analyses which have employed different methods of ascertainment, and tends to confirm that a proportion of GTS is due to a dominant gene and is suitable for investigation with genetic markers for linkage analysis.
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