Dev Psychopathol 2015[Nov]; 27 (4 Pt 2): 1637-45 PMID26535949show ga
A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families, including n=69 with child welfare documentation of moderate-severe maltreatment in the past six months, participated in this study. Children ranged in age from 3 to 5 years, and were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors, and a composite variable assessed the number exposures to these adversities. Methylation of two CpG sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p<.05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p<.05). FKBP5 alters glucocorticoid receptor responsiveness and FKBP5 gene methylation may be a mechanism of the bio-behavioral effects of adverse exposures in young children.
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Dev+Psychopathol 2015 ; 27 (4 Pt 2): 1637-45
