Highlights
- •Plasma BDNF levels do not differ between controls and patients with depression.
- •Plasma BDNF levels do not change following a course of ECT.
- •Patients with Val/Met or Met/Met genotype have higher BDNF levels than Val/Val.
- •Plasma BDNF levels are not related to depression symptom severity.
- •Plasma BDNF levels are not associated with the therapeutic response to ECT.
Abstract
Background
Brain derived neurotrophic factor (BDNF) has been implicated in the pathophysiology
of depression and the antidepressant response. Electroconvulsive therapy (ECT) is
reported to increase BDNF levels in blood, though only a small number of studies have
been conducted to date.
Objective
Our objectives were to: 1) compare plasma BDNF levels in medicated patients with depression
and controls; 2) assess the effect of ECT on plasma BDNF levels in medicated patients
with depression; 3) explore the relationship between plasma BDNF levels and the Val66Met
(rs6265) BDNF polymorphism; and 4) examine the relationship between plasma BDNF levels and clinical
symptoms and outcomes with ECT.
Methods
Plasma BDNF levels were analyzed in samples from 61 medicated patients with a major
depressive episode and 50 healthy controls, and in patient samples following a course
of ECT. Fifty-two samples from the depressed patient group were genotyped for the
Val66Met BDNF polymorphism.
Results
There was no difference in plasma BDNF levels between the control and depressed groups,
and there was no difference in plasma BDNF levels in patients following treatment
with ECT. In line with previous reports, we show that, in medicated patients with
depression, Met-carriers had higher plasma BDNF levels than Val-carriers, though genotype
was not related to clinical response. We found no association between plasma BDNF
levels and depression severity or the clinical response to ECT.
Conclusions
Our results suggest that plasma BDNF does not represent a suitable candidate biomarker
for determining the therapeutic response to ECT.
Keywords
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Article info
Publication history
Published online: May 18, 2018
Accepted:
May 15,
2018
Received in revised form:
April 30,
2018
Received:
January 19,
2018
Identification
Copyright
© 2018 Elsevier Inc. All rights reserved.