Plaisance T A C Reydon Eds Philosophy of behavioral biology pp 4364 Dordrecht

Plaisance t a c reydon eds philosophy of behavioral

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Plaisance & T. A. C. Reydon (Eds.), Philosophy of behavioral biology (pp. 43–64). Dordrecht, The Netherlands: Springer. Turkheimer, E., Pettersson, E., & Horn, E. E. (2014). A phenotypic null hypothesis for the genetics of personality. Annual Review of Psychology , 65 , 515–540. Visscher, P. M., Brown, M. A., McCarthy, M. I., & Yang, J. (2012). Five years of GWAS discovery. American Journal of Human Genetics , 90 , 7–24. Walsh, K. M., Anderson, E., Hansen, H. M., Decker, P. A., Kosel, M. L., Kollmeyer, T., … Wrensch, M. R. (2013). Analysis of 60 reported glioma risk SNPs replicates published GWAS findings but fails to replicate associations from published candidate-gene studies. Genetic Epidemiology, 37, 222–228. Wood, A. R., Esko, T., Yang, J., Vedantam, S., Pers, T. H., … Frayling, T. M. (2014). Defining the role of common variation in the genomic and biological architecture of adult human height. Nature Genetics , 46 , 1173–1186.
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THE FOURTH LAW OF BEHAVIOR GENETICS 25 Wray, N. R., Purcell, S. M., & Visscher, P. M. (2011). Synthetic associations created by rare variants do not explain most GWAS results. PLoS Biology , 9 , e1000579. Yang, J., Benyamin, B., McEvoy, B., Gordon, S., Henders, A.K., Nyholt, D.R., … Visscher, P.M. (2010). Common SNPs explain a large proportion of the heritability for human height. Nature Genetics , 42 , 565–569.
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THE FOURTH LAW OF BEHAVIOR GENETICS 26 Figure 1 . Number of schizophrenia-associated SNPs clearing the strict GWAS significance threshold ( p < 5 × 10 –8 ) as a function of discovery-stage sample size, which has increased over time. Although the four studies presented are not methodologically identical (because of different ratios of cases to controls), the increasing number of “hits” with sample size is nevertheless informative.
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THE FOURTH LAW OF BEHAVIOR GENETICS 27 Figure 2 . Estimated total number of SNPs associated with five disease phenotypes based on results of genome-wide association studies (based on a figure in Ripke et al., 2013). rheumatoid arthritis celiac disease coronary artery disease type 2 diabetes schizophrenia ESTIMATED NUMBER OF TRAIT-ASSOCIATED MARKERS 0 2000 4000 6000 8000
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THE FOURTH LAW OF BEHAVIOR GENETICS 28 Figure 3. The strong agreement between genetic effects on 28 diseases estimated in Europeans and East Asians (reproduced from Marigorta & Navarro, 2013). The x -axis corresponds to the increment in the odds (on a logarithmic scale) of suffering from the disease for each additional copy of the reference allele, as estimated in Europeans. The y -axis corresponds to the same quantity estimated in East Asians. The increment in log(odds) is the equivalent of the “additive effect” for dichotomously scored traits such as disease status (affected versus unaffected). The gap in the data on the x -axis results from the fact that non-significant genetic effects would have odds ratios near 1 (and thus logarithms of 0) and therefore would not be included in the results of European samples.
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