Abstract
FKBP5 gene variants may predict antidepressant treatment response in individuals with Major Depressive Disorder. PubMed and Web of Science were searched systematically for articles studying individuals who had received a diagnosis of Major Depressive Disorder (MDD) and were given antidepressant treatment. Inclusion criteria were studies that researched FKBP5 and its variants and focused on antidepressant treatment response. Previous studies support a potential underlying epigenetic mechanism, demethylation at FKBP5 polymorphisms (rs1360780, rs3800373, rs9470080, and rs4713916) after experiencing childhood trauma, leading to increased hypothalamic-pituitary-adrenal (HPA) axis sensitivity and a propensity for the development of MDD. These polymorphisms informed the search, but additional polymorphisms (rs9380514, rs352428) were also considered. Studies conducted prior to 2008, reviews, meta-analyses, editorials, and non-research based articles were excluded. Studies examined in this article link FKBP5 polymorphisms (rs4713916) and FKBP5 RNA levels with positive antidepressant response. Variants rs1360780, rs3800373, and rs9470080 were associated with both positive response and non-response or lack of remission. Variants rs9380514, rs352428, and rs936882 were associated with poor response to antidepressant treatment or non-remission. Further insights into the role FKBP5 plays in development and antidepressant treatment response may be aided by future studies focused on individuals who previously experienced childhood trauma and later developed MDD.
Highlights
In 2018, approximately 17.7 million adults in the United States had suffered at least one major depressive episode,[1] and a survey conducted by the Centers for Disease Control and Prevention (CDC) estimated 12.7 percent of Americans aged 12 and over took antidepressant medication within the past month.[2]
FK506 binding protein 5 (FKBP5) polymorphisms associated with childhood trauma and development of Major Depressive Disorder (MDD) were of particular interest, but polymorphisms that did not meet these criteria were included
Articles that were considered out-of-scope of this review included studies that used non-human models with a focus on neuronal differentiation, studies that focused on the interaction between FKBP5 and other genes, and those that focused on FKBP5 variants and their impact on conditions other than MDD
Summary
In 2018, approximately 17.7 million adults in the United States had suffered at least one major depressive episode,[1] and a survey conducted by the Centers for Disease Control and Prevention (CDC) estimated 12.7 percent of Americans aged 12 and over took antidepressant medication within the past month.[2] Antidepressants used to treat Major Depressive Disorder (MDD) have historically varied in efficacy for different individuals. Prescription of these medications is often on a trial-and-error basis, potentially delaying effective treatment for patients. Recent studies indicate that there may be several origins and subtypes of MDD, suggesting that a more appropriate subpopulation for genetic studies may be identified by a shared experience or other factors contributing to MDD development.[7,8]
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