Brain-derived neurotrophic factor as a possible predictor of electroconvulsive therapy outcome

Abstract

While brain-derived neurotrophic factor (BDNF) has been shown to predict response to pharmacotherapy in depression, studies in electroconvulsive therapy (ECT) are small and report conflicting results. This study assesses the association between pre-treatment BDNF levels and ECT outcome in severe late-life unipolar depression (LLD). The potential of BDNF as a clinical predictor of ECT outcome was subsequently evaluated. Characteristics associated with low and high BDNF subgroups were determined as well. Ninety-four patients diagnosed with LDD referred for ECT were included. Fasting serum BDNF levels were determined before ECT. Remission and response, measured with the Montgomery–Åsberg Depression Rating Scale, were the outcomes. The association between BDNF and ECT outcome was analysed with logistic regression and Cox regression. The clinical usefulness of BDNF was evaluated using the receiver operating characteristic (ROC) curve. Associations between clinical characteristics and low versus high BDNF levels were examined with T tests, chi-squared tests and Mann−Whitney tests. The odds of remission decreased with 33% for every five units increase of BDNF levels (OR 0.67, 95% confidence interval 0.47–0.96; p = 0.03); however, neither the association with time to remission nor the associations with response nor the adjusted models were significant. The area under the ROC (0.66) implied a poor accuracy of BDNF as a clinical test. Clinical characteristics associated with BDNF were inclusion site, physical comorbidities and duration of the index episode. To conclude, although there is an association between pre-treatment BDNF levels and ECT outcome, BDNF cannot be considered an eligible biomarker for ECT outcome in clinical practice.

<p>BDNF and the Antidepressant Effects of Ketamine and Propofol in Electroconvulsive Therapy: A Preliminary Study</p>

“…Numerous studies have investigated the effect of ECT on serum levels of BDNF in patients with MDD. 22,[28][29][30][31][32][33] Consistent with our findings, earlier studies also found that ECT could not alter serum levels of BDNF, despite decreasing depression severity. [28][29][30][31]33,34 This indicates that ECT probably does not share a common mechanism of action as antidepressants in the improvement of depressive symptoms for patients with TRD.…”

“…A perennial question among researchers is whether it is more correct to measure BDNF levels in plasma, serum or whole blood. BDNF is known to be stored in human platelets and to circulate in plasma, 22 but BDNF concentration in plasma is affected by the handling of the blood sample, and it is released upon platelet degranulation. Thus, circulating BDNF is usually measured in the serum.…”

Serum BDNF levels and the antidepressant effects of electroconvulsive therapy with ketamine anaesthesia: a preliminary study

“…Similar to nonconvulsive electrotherapy (NET) using standard ECT technique but below seizure threshold, the change in serum BDNF levels in patients with TRD was not correlated with the antidepressant effects of NET ( Zheng et al, 2020 ). A recent study concluded that serum BDNF levels in patients with late-life unipolar depression cannot be considered an eligible biomarker for the antidepressant effects of ECT ( Van Zutphen et al, 2019 ).…”

The Diagnostic Value of the Combination of Serum Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor-1 for Major Depressive Disorder Diagnosis and Treatment Efficacy

“…However, recent works have shown that not all antidepressants increase BDNF concentrations ( 47 ), and antidepressant-induced rise in BDNF concentrations are more substantial in responders compared to non-responders ( 48 – 51 ). Moreover, it was demonstrated that high-intensity exercises ( 52 ), electroconvulsive therapy ( 15 , 18 , 19 , 53 ), and deep brain stimulation ( 54 ) also increase BDNF levels. In animal studies, it has been revealed that vortioxetine enhances the behaviors of depressed rodents probably by influencing the cAMP/CREB/BDNF signal pathway and promoting the expression of BDNF in the dorsal and ventral hippocampus of the animals ( 55 , 56 ).…”