<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Srinivasan, Saurabh</style></author><author><style face="normal" font="default" size="100%">Bettella, Francesco</style></author><author><style face="normal" font="default" size="100%">Mattingsdal, Morten</style></author><author><style face="normal" font="default" size="100%">Wang, Yunpeng</style></author><author><style face="normal" font="default" size="100%">Witoelar, Aree</style></author><author><style face="normal" font="default" size="100%">Schork, Andrew J.</style></author><author><style face="normal" font="default" size="100%">Thompson, Wesley K.</style></author><author><style face="normal" font="default" size="100%">Zuber, Verena</style></author><author><style face="normal" font="default" size="100%">Winsvold, Bendik S.</style></author><author><style face="normal" font="default" size="100%">Zwart, John-Anker</style></author><author><style face="normal" font="default" size="100%">Collier, David A.</style></author><author><style face="normal" font="default" size="100%">Desikan, Rahul S.</style></author><author><style face="normal" font="default" size="100%">Melle, Ingrid</style></author><author><style face="normal" font="default" size="100%">Werge, Thomas</style></author><author><style face="normal" font="default" size="100%">Dale, Anders M.</style></author><author><style face="normal" font="default" size="100%">Djurovic, Srdjan</style></author><author><style face="normal" font="default" size="100%">Andreassen, Ole A.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genetic Markers of Human Evolution Are Enriched in Schizophrenia</style></title><secondary-title><style face="normal" font="default" size="100%">Biological PsychiatryBiological Psychiatry</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2016</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.biologicalpsychiatryjournal.com/article/S0006-3223(15)00855-0/abstract</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">80</style></volume><pages><style face="normal" font="default" size="100%">284 - 292</style></pages><isbn><style face="normal" font="default" size="100%">0006-3223</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Why schizophrenia has accompanied humans throughout our history despite its negative effect on fitness remains an evolutionary enigma. It is proposed that schizophrenia is a by-product of the complex evolution of the human brain and a compromise for humans? language, creative thinking, and cognitive abilities.&lt;/p&gt;

&lt;p&gt;We analyzed recent large genome-wide association studies of schizophrenia and a range of other&lt;br /&gt;
human phenotypes (anthropometric measures, cardiovascular disease risk factors, immune-mediated diseases)&lt;br /&gt;
using a statistical framework that draws on polygenic architecture and ancillary information on genetic variants.&lt;br /&gt;
We used information from the evolutionary proxy measure called the Neanderthal selective sweep (NSS) score.&lt;/p&gt;

&lt;p&gt;Gene loci associated with schizophrenia are significantly (p 5 7.30 3 1029) more prevalent in genomic&lt;br /&gt;
regions that are likely to have undergone recent positive selection in humans (i.e., with a low NSS score). Variants in&lt;br /&gt;
brain-related genes with a low NSS score confer significantly higher susceptibility than variants in other brain-related&lt;br /&gt;
genes. The enrichment is strongest for schizophrenia, but we cannot rule out enrichment for other phenotypes.&lt;br /&gt;
The false discovery rate conditional on the evolutionary proxy points to 27 candidate schizophrenia susceptibility&lt;br /&gt;
loci, 12 of which are associated with schizophrenia and other psychiatric disorders or linked to brain development.&lt;/p&gt;

&lt;p&gt;Our results suggest that there is a polygenic overlap between schizophrenia and NSS score, a&lt;br /&gt;
marker of human evolution, which is in line with the hypothesis that the persistence of schizophrenia is related to the&lt;br /&gt;
evolutionary process of becoming human.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><notes><style face="normal" font="default" size="100%">&lt;p&gt;doi: 10.1016/j.biopsych.2015.10.009&lt;/p&gt;
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