Serum BDNF as a peripheral biomarker of treatment-resistant depression and the rapid antidepressant response: A comparison of ketamine and ECT

Aug 16, 2015Journal of affective disorders

Blood BDNF levels linked to hard-to-treat depression and quick antidepressant responses to ketamine and ECT

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Abstract

Serum brain-derived neurotrophic factor (sBDNF) was significantly elevated only one week after the first ketamine infusion in responders.

Patients with treatment-resistant depression (TRD) had lower levels of sBDNF at baseline compared to healthy controls.
Both ketamine infusions and electroconvulsive therapy (ECT) were linked to significant reductions in depressive symptoms.
The increase in sBDNF levels was observed only after the first ketamine infusion and not after subsequent infusions.
ECT did not result in an increase in sBDNF despite reducing depressive symptoms.
Normalizing sBDNF levels does not seem necessary for achieving symptom improvement in TRD with either ketamine or ECT.

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BACKGROUND: Ketamine is associated with rapid antidepressant efficacy but the biological mechanisms underpinning this effect are unclear. Serum brain-derived neurotrophic factor (sBDNF) is a potential circulating biomarker of treatment-resistant depression (TRD) and ketamine response but it is unclear if this is a common target of both ketamine and electroconvulsive therapy (ECT), the current gold standard for TRD. Moreover, the impact of multiple ketamine infusions on sBDNF has not yet been established.

METHODS: Thirty five TRD patients with a current DSM-IV diagnosis of recurrent depressive disorder received up to 12 ECT sessions (N=17) or up to three intravenous infusions of low-dose (0.5mg/kg) ketamine (N=18). Blood samples were taken over the course of the study for assessment of sBDNF. Symptom severity and response were monitored using the 17-item Hamilton Depression Rating Scale (HDRS). sBDNF was assessed in 20 healthy controls to allow comparison with TRD patients.

RESULTS: As expected, sBDNF was lower in TRD patients at baseline compared to healthy controls. Ketamine and ECT treatment were both associated with significant reductions in depressive symptoms. However, sBDNF was significantly elevated only at one week following the first ketamine infusion in those classified as responders one week later. sBDNF was not elevated following subsequent infusions. ECT reduced depressive symptoms, as expected, but was not associated with an enhancement in BDNF.

LIMITATIONS: Patients continued with their psychotropic medications throughout this trial.

CONCLUSIONS: SBDNF normalisation does not appear to be a prerequisite for symptomatic improvement in TRD following ketamine or ECT treatment.

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Serum BDNF as a peripheral biomarker of treatment-resistant depression and the rapid antidepressant response: A comparison of ketamine and ECT

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