Browsing by Subject "Heritability"

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Open Access
Heritability of neuropsychological measures in schizophrenia and nonpsychiatric populations: a systematic review and meta-analysis
(Oxford University Press, 2017) Blokland, G. A. M.; Mesholam-Gately, R. I.; Toulopoulou, T.; Del Re, E. C.; Lam, M.; Delisi, L. E.; Donohoe, G.; Walters, J. T. R.; Seidman, L. J.; Petryshen, T. L.
Schizophrenia is characterized by neuropsychological deficits across many cognitive domains. Cognitive phenotypes with high heritability and genetic overlap with schizophrenia liability can help elucidate the mechanisms leading from genes to psychopathology. We performed a meta-analysis of 170 published twin and family heritability studies of >800 000 nonpsychiatric and schizophrenia subjects to accurately estimate heritability across many neuropsychological tests and cognitive domains. The proportion of total variance of each phenotype due to additive genetic effects (A), shared environment (C), and unshared environment and error (E), was calculated by averaging A, C, and E estimates across studies and weighting by sample size. Heritability ranged across phenotypes, likely due to differences in genetic and environmental effects, with the highest heritability for General Cognitive Ability (32%-67%), Verbal Ability (43%-72%), Visuospatial Ability (20%-80%), and Attention/Processing Speed (28%-74%), while the lowest heritability was observed for Executive Function (20%-40%). These results confirm that many cognitive phenotypes are under strong genetic influences. Heritability estimates were comparable in nonpsychiatric and schizophrenia samples, suggesting that environmental factors and illness-related moderators (eg, medication) do not substantially decrease heritability in schizophrenia samples, and that genetic studies in schizophrenia samples are informative for elucidating the genetic basis of cognitive deficits. Substantial genetic overlap between cognitive phenotypes and schizophrenia liability (average r g = '.58) in twin studies supports partially shared genetic etiology. It will be important to conduct comparative studies in well-powered samples to determine whether the same or different genes and genetic variants influence cognition in schizophrenia patients and the general population.
Open Access
Integrating molecular genetics and evolutionary psychology: Sexual jealousy and the androgen receptor (AR) gene
(Elsevier, 2018) Lewis, D. M. G.; Al-Shawaf, L.; Janiak, M. C.; Akunebu, S. P.
Integrating evolutionary psychological and molecular genetic research may increase our knowledge of the psychological correlates of specific genes, as well as enhance evolutionary psychology's ability to explain individual differences. We tested the hypothesis that men's sexual jealousy mechanisms functionally calibrate their psychological output according to genetic variation at the androgen receptor locus. Mated men (N = 103) provided buccal cell samples for genotype fragment analysis and completed inventories assessing their sexually jealous cognitions and emotions. Results indicated that men with longer sequences of CAG codon repeats at the androgen receptor locus were more likely to perceive ambiguous social and environmental cues as indicative of their mates’ infidelity, and experienced greater emotional upset in response to these cues. These results contribute to a growing body of research linking polymorphism at the AR locus to individual differences in psychology, and, to our knowledge, provide the first evidence pointing toward the heritability of sexual jealousy. Our discussion centers on whether the heritability of psychological differences implies direct genetic influences on the neurobiological substrate, or reflects functionally calibrated output from sex-typical and species-typical mechanisms. We conclude by describing how future research can more clearly differentiate between these alternative genetic models.