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Glucocorticoid Receptor Polymorphisms in Major Depression
Author(s) -
Spijker Anne T.,
van Rossum Elisabeth F. C.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04985.x
Subject(s) - glucocorticoid receptor , mood disorders , mineralocorticoid receptor , medicine , bipolar disorder , major depressive disorder , endocrinology , depression (economics) , psychology , glucocorticoid , mood , polymorphism (computer science) , cognition , receptor , neuroscience , clinical psychology , psychiatry , genotype , biology , genetics , gene , anxiety , economics , macroeconomics
Previously, it has been suggested that hypothalamic‐pituitary‐adrenal (HPA) axis dysregulation and, as a consequence, increased cortisol levels, is not only a state phenomenon, but may also be a trait phenomenon in mood disorders. Cortisol exerts its effects mainly by binding to the glucocorticoid receptor (GR) and, of particular interest in certain brain regions, the mineralocorticoid receptor (MR). Several GR polymorphisms have been shown to be associated with altered sensitivity of the HPA axis. Recently, the GR polymorphisms Bcl I and ER22/23EK have been associated with unipolar depression in several studies. In addition, the ER22/23EK polymorphism seems to be associated with a decreased risk of dementia in healthy individuals. Also, during a depressive episode, carriers of this ER22/23EK variant demonstrated a tendency toward better cognition, as measured by divided attention tests. In this overview, currently known clinically relevant GR and MR polymorphisms are discussed in relation to mood disorders (both unipolar depression and bipolar disorder) and cognitive function.