2021
DOI: 10.3389/fpsyt.2021.642245
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Corrigendum: Methylation of FKBP5 and SLC6A4 in Relation to Treatment Response to Mindfulness Based Stress Reduction for Posttraumatic Stress Disorder

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Cited by 2 publications
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“…FKBP5 modulates glucocorticoid receptor activity in response to stress [ 38 ]. This finding contradicts those by Creswell et al (2012), who found downregulation of FKBP5 after mindfulness-based stress reduction, and by Bishop et al [ [39] , [40] ] who found increased methylation of the FKBP5 gene in individuals with PTSD who responded to a mindfulness-based stress reduction intervention compared to non-responders. Again, further research will be needed to determine whether these discrepancies are due to differences in the intensity or style of practice, individual differences (e.g., in mental health profiles), or other environmental factors.…”
Section: Discussioncontrasting
confidence: 58%
“…FKBP5 modulates glucocorticoid receptor activity in response to stress [ 38 ]. This finding contradicts those by Creswell et al (2012), who found downregulation of FKBP5 after mindfulness-based stress reduction, and by Bishop et al [ [39] , [40] ] who found increased methylation of the FKBP5 gene in individuals with PTSD who responded to a mindfulness-based stress reduction intervention compared to non-responders. Again, further research will be needed to determine whether these discrepancies are due to differences in the intensity or style of practice, individual differences (e.g., in mental health profiles), or other environmental factors.…”
Section: Discussioncontrasting
confidence: 58%
“…At present, the neurobiological mechanism of PTSD has not been confirmed, and the research directions mainly include four aspects: (1) Genes involved with monoamine and the hypothalamic-pituitary-adrenal (HPA) axis function have been examined extensively in epigenetic and genetic studies of PTSD risk and separately in studies of disease risk and response to treatments for mood disorders ( Kato and Serretti, 2010 ; Domschke et al, 2014 ; Zannas et al, 2015 ; Smoller, 2016 ). Two of the most commonly characterized genes in this regard are the serotonin transporter (SLC6A4) and FK506 binding protein 5 (FKBP5) ( Bishop et al, 2021 ); (2) neuroendocrine dysfunction, such as the increased secretion of catecholamines ( Olson et al, 2011 ) and decreased secretion of 5-hydroxytryptamine (5-HT) hormones ( Liu et al, 2018 ) and corticosterone ( Geracioti et al, 2008 ); (3) changes in the neural structure and circuitry. Basic and clinical studies have demonstrated that structural and functional abnormalities in the hippocampus, prefrontal cortex (PFC), amygdala, and other brain areas were observed in both animal models and individuals with PTSD ( Rauch et al, 2006 ; Hayes et al, 2012 ; Disner et al, 2018 ).…”
Section: Introductionmentioning
confidence: 99%