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Genetic mechanisms of electroconvulsive therapy response in depression
Author(s) -
BensonMartin Janine J.,
Stein Dan J.,
Baldwin David S.,
Domschke Katharina
Publication year - 2016
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.2531
Subject(s) - electroconvulsive therapy , neurotrophic factors , psychology , apolipoprotein e , depression (economics) , neuroscience , bioinformatics , clinical psychology , medicine , psychiatry , cognition , biology , receptor , disease , economics , macroeconomics
Electroconvulsive therapy (ECT) is known to be one of the most effective treatments for managing depression and other severe mental illnesses. Nevertheless, the exact mechanisms underlying response to ECT remain uncertain. This mini‐review presents clinical findings regarding the role of genetic factors in the aetiology of the ECT response. Studies on the role of variation in the catechol‐ O ‐methyltransferase ( COMT ) gene; other dopamine‐, serotonin‐, and G‐protein‐related genes; brain‐derived neurotrophic factor (BDNF); apolipoprotein E (APOE); angiotensin I‐converting enzyme (ACE) and vascular endothelial growth factor (VEGF) genes in mediating response to ECT are summarized. The existing data support the notion that some genetic factors—particularly the functional COMT val158met polymorphism—may play a role in the magnitude of clinical response to ECT, and thus could serve as potential biomarkers for future personalized treatment approaches. However, much of the work to date is preliminary, and large‐scale confirmatory studies are still needed. Copyright © 2016 John Wiley & Sons, Ltd.