The interaction of serotonin transporter gene polymorphisms and early adverse life events on vulnerability for major depression.
Considerable literature supports the hypothesis of dysfunction in central nervous system serotonergic circuits in the pathophysiology of mood disorders, specifically major depression. Since the development of the selective serotonin (5-HT) reuptake inhibitors, a putative role for the 5-HT transporter (SERT) in the etiology of depression has been explored. The discovery of a functional SERT polymorphism has provided a novel tool to further scrutinize the role of serotonergic neurons in depression. This article reviews the burgeoning evidence of an interaction between early life stress and an SERT polymorphism on vulnerability to depression.
Vergne
Derick E
DE
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Suite 4000 WMRB, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Nemeroff
Charles B
CB
D000818:Animals; D000928:Antidepressive Agents / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D003865:Major Depressive Disorder / Q000188:drug therapy / Q000235:genetics* / Q000523:psychology; D005838:Genotype; D006801:Humans; D008016:Life Change Events; D051379:Mice; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors; D050486:Serotonin Plasma Membrane Transport Proteins / Q000187:drug effects / Q000235:genetics*
D000928:Antidepressive Agents; C493230:SLC6A4 protein, human; D050486:Serotonin Plasma Membrane Transport Proteins