A success at the end of an era, and a glimpse of things to come

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The history of genetic studies of bipolar disorder can be divided into eras distinguished by the methodology that drove the big advances. The first era started roughly with Kraepelin in the 1890s; it rested on descriptive phenomenology and established the definition of what geneticists call the bipolar phenotype. The second era started with the early twin studies in the 1930s and relied on genetic epidemiology to show that bipolar disorder was largely a genetic disease. The third era, which we can call the linkage era, probably began with the first genetic linkage study of bipolar disorder in the late 1960s but did not really get under way until molecular markers became available for genetic mapping in the late 1980s. The linkage era is now passing and may soon be overshadowed by the findings that are emerging from genetic association studies, especially the genome-wide studies that will come to dominate the field in the coming years. In this issue of the American Journal of Psychiatry, Jones et al. have shown that yet another clinical feature, in this case postpartum or puerperal onset, substantially increases linkage evidence to regions of chromosomes 16 and 8 that have been implicated in other studies. Also in this issue, Matsuzawa et al. provide a taste of the power of genetic association studies to detect alleles that contribute to psychiatric disease, in this case, methamphetamine psychosis. The candidate gene approach may follow linkage approaches into obsolescence as denser sets of markers for genome-wide association studies become available, but there will probably always be room for good hypothesis-driven candidate gene studies, especially for phenotypes that might not easily provide the large sample sizes needed for genome-wide studies. (PsycINFO Database Record (c) 2016 APA, all rights reserved)

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