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Amygdala responses to quetiapine XR and citalopram treatment in major depression: the role of 5‐HTTLPR‐S/Lg polymorphisms
Author(s) -
Ramasubbu Rajamannar,
Burgess Ashley,
GaxiolaValdez Ismael,
Cortese Filomeno,
Clark Darren,
Kemp Anne,
Goodyear Bradley,
Macqueen Glenda,
BechHansen N. Torben,
Foster Jane,
Diwadkar Vaibhav A.
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.2521
Subject(s) - quetiapine , citalopram , amygdala , major depressive disorder , antidepressant , quetiapine fumarate , psychology , 5 httlpr , serotonin transporter , medicine , oncology , neuroimaging , psychiatry , serotonin , schizophrenia (object oriented programming) , hippocampus , antipsychotic , atypical antipsychotic , receptor
Objectives Genotype and drug pharmacology may contribute to variations in brain response to antidepressants. We examined the impact of two antidepressants with differential actions on serotonin transporter and the 5‐HHTLPR‐S/Lg polymorphisms on amygdala responses in major depressive disorder (MDD). Methods Caucasians with MDD were given either citalopram or quetiapine extended release for 8 weeks. Patients were genotyped for 5‐HTTLPR. Clinical efficacy was assessed using the Hamilton Depression Rating Scale. fMRI responses to negative emotional faces were acquired at baseline, week 1 and week 8. The outcome measure was change in amygdala responses at week 8. Results Citalopram had no effect on amygdala responses in MDD patients with S/Lg alleles at weeks 1 and 8 compared with baseline, whereas it induced changes in amygdala responses in LL homozygotes. By contrast, quetiapine decreased amygdala responses at both time points in S/Lg carriers, and changes in amygdala responses at week 8 correlated with a reduction in depression scores. The small number of LL homozygotes in quetiapine group was a limitation. Efficacy of both treatments was comparable. Conclusions These preliminary data suggest that pharmacological mechanisms and genetics need to be considered in the development of neuroimaging markers for the evaluation of antidepressant treatments. Copyright © 2016 John Wiley & Sons, Ltd.