TY - JOUR
T1 - Investigating the potential role of BDNF and PRL genotypes on antidepressant response in depression patients
T2 - A prospective inception cohort study in treatment-free patients
AU - Ochi, Taichi
AU - Vyalova, Natalya M.
AU - Losenkov, Innokentiy S.
AU - Levchuk, Lyudmila A.
AU - Osmanova, Diana Z.
AU - Mikhalitskaya, Ekaterina V.
AU - Loonen, Anton J.M.
AU - Bosker, Fokko J.
AU - Simutkin, German G.
AU - Bokhan, Nikolay A.
AU - Wilffert, Bob
AU - Ivanova, Svetlana A.
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Background: Brain-derived neurotrophic factor (BDNF) is associated with response to antidepressant drugs in mood and anxiety disorders. Prolactin (PRL) is a pituitary hormone with behavioural effects, acting as a neurotrophic factor within the brain and may be involved in antidepressant response. Objectives: To investigate the relationship between BDNF and PRL genotypes with antidepressant drug response. Methods: Prospective inception cohort of 186 Russian treatment-free participants (28 men and 158 women) between 18 and 70 years clinically diagnosed with depressive disorder who initiated antidepressant medication. DNA polymorphisms were genotyped for PRL rs1341239, BDNF rs6265 and rs7124442. Primary outcome was measured by differences in Hamilton Depression Rating Scale (∆HAM-D) scores between baseline/week two, week two/week four, and baseline/week four. Linear regression and independent t-test determined the significance between polymorphisms and ∆HAM-D. Results: Comparisons between genotypes did not reveal any significant differences in scores during the first two weeks of treatment. In the latter two weeks, BDNF rs7124442 homozygous C patients responded significantly worse in comparison to homozygous T patients during this period. Further analysis within women and in post-menopausal women found a similar comparison between alleles. Limitations: Study lasted four weeks, which may be considered short to associate genuine antidepressant effects. Conclusions: Patients taking tricylic antidepressants were noted to have a significant improvement in ∆HAM-D compared to patients taking SSRIs. Homozygous C BDNF rs712442 patients were found to respond significantly worse in the last two weeks of treatment.
AB - Background: Brain-derived neurotrophic factor (BDNF) is associated with response to antidepressant drugs in mood and anxiety disorders. Prolactin (PRL) is a pituitary hormone with behavioural effects, acting as a neurotrophic factor within the brain and may be involved in antidepressant response. Objectives: To investigate the relationship between BDNF and PRL genotypes with antidepressant drug response. Methods: Prospective inception cohort of 186 Russian treatment-free participants (28 men and 158 women) between 18 and 70 years clinically diagnosed with depressive disorder who initiated antidepressant medication. DNA polymorphisms were genotyped for PRL rs1341239, BDNF rs6265 and rs7124442. Primary outcome was measured by differences in Hamilton Depression Rating Scale (∆HAM-D) scores between baseline/week two, week two/week four, and baseline/week four. Linear regression and independent t-test determined the significance between polymorphisms and ∆HAM-D. Results: Comparisons between genotypes did not reveal any significant differences in scores during the first two weeks of treatment. In the latter two weeks, BDNF rs7124442 homozygous C patients responded significantly worse in comparison to homozygous T patients during this period. Further analysis within women and in post-menopausal women found a similar comparison between alleles. Limitations: Study lasted four weeks, which may be considered short to associate genuine antidepressant effects. Conclusions: Patients taking tricylic antidepressants were noted to have a significant improvement in ∆HAM-D compared to patients taking SSRIs. Homozygous C BDNF rs712442 patients were found to respond significantly worse in the last two weeks of treatment.
KW - Antidepressant response
KW - Brain derived neurotrophic factor
KW - Major depressive disorder
KW - Prolactin
KW - rs6265
KW - rs7124442
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U2 - 10.1016/j.jad.2019.08.058
DO - 10.1016/j.jad.2019.08.058
M3 - Article
AN - SCOPUS:85071718271
VL - 259
SP - 432
EP - 439
JO - Journal of Affective Disorders
JF - Journal of Affective Disorders
SN - 0165-0327
ER -