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Common polymorphisms in the human gene for <jats:styled-content style=\"fixed-case\">FK506<\/jats:styled-content> binding protein 5 (<jats:italic><jats:styled-content style=\"fixed-case\">FKBP5<\/jats:styled-content><\/jats:italic>), which is involved in transcriptional regulation of the hypothalamic\u2013pituitary\u2013adrenal (<jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content>) axis, have been shown to interact with childhood abuse and trauma to predict stress\u2010related psychopathology. In the current study, we examined if such gene\u2013environment interaction effects may be related to variability in the threat\u2010related reactivity of the amygdala, which plays a critical role in mediating physiological and behavioral adaptations to stress including modulation of the <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content> axis. To this end, 139 healthy Caucasian youth completed a blood oxygen level\u2010dependent functional magnetic resonance imaging probe of amygdala reactivity and self\u2010report assessments of emotional neglect (<jats:styled-content style=\"fixed-case\">EN<\/jats:styled-content>) and other forms of maltreatment. These individuals were genotyped for 6 <jats:italic><jats:styled-content style=\"fixed-case\">FKBP5<\/jats:styled-content><\/jats:italic> polymorphisms (rs7748266, rs1360780, rs9296158, rs3800373, rs9470080 and rs9394309) previously associated with psychopathology and\/or <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content> axis function. Interactions between each <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">EN<\/jats:styled-content> emerged such that risk alleles predicted relatively increased dorsal amygdala reactivity in the context of higher <jats:styled-content style=\"fixed-case\">EN<\/jats:styled-content>, even after correcting for multiple testing. Two different haplotype analyses confirmed this relationship as haplotypes with risk alleles also exhibited increased amygdala reactivity in the context of higher <jats:styled-content style=\"fixed-case\">EN<\/jats:styled-content>. Our results suggest that increased threat\u2010related amygdala reactivity may  represent a mechanism linking psychopathology to interactions between common genetic variants affecting <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content> axis function and childhood trauma<\/jats:bold>.<\/jats:p>","DOI":"10.1111\/j.1601-183x.2012.00837.x","type":"journal-article","created":{"date-parts":[[2012,9,15]],"date-time":"2012-09-15T09:22:28Z","timestamp":1347700948000},"page":"869-878","source":"Crossref","is-referenced-by-count":166,"title":["<i><scp>FKBP5<\/scp><\/i> and emotional neglect interact to predict individual differences in amygdala reactivity"],"prefix":"10.1111","volume":"11","author":[{"given":"M. G.","family":"White","sequence":"first","affiliation":[{"name":"Laboratory of NeuroGenetics, Department of Psychology &amp; Neuroscience Duke University  Durham NC USA"},{"name":"Lieber Institute for Brain Development  Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Bogdan","sequence":"additional","affiliation":[{"name":"Laboratory of NeuroGenetics, Department of Psychology &amp; Neuroscience Duke University  Durham NC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. M.","family":"Fisher","sequence":"additional","affiliation":[{"name":"Center for Integrated Molecular Brain Imaging Neurobiology Research Unit  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. E.","family":"Mu\u00f1oz","sequence":"additional","affiliation":[{"name":"Department of Psychology University of Pittsburgh  Pittsburgh PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. 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