Plasma Brain-Derived Neurotrophic Factor Levels Predict the Clinical Outcome of Depression Treatment in a Naturalistic Study

Abstract

Remission is the primary goal of treatment for major depressive disorder (MDD). However, some patients do not respond to treatment. The main purpose of this study was to determine whether brain-derived neurotrophic factor (BDNF) levels are correlated with treatment outcomes. In a naturalistic study, we assessed whether plasma BDNF levels were correlated with clinical outcomes by measuring plasma BDNF in patients with depressive syndrome (MADRS score ≥18), and subsequently comparing levels between the subgroup of patients who underwent remission (MADRS score ≤8) and the subgroup who were refractory to treatment (non-responders). Patients with depressive syndrome who underwent remission had significantly higher plasma BDNF levels (p<0.001), regardless of age or sex. We also found a significant negative correlation between MADRS scores and plasma BDNF levels within this group (ρ = –0.287, p = 0.003). In contrast, non-responders had significantly lower plasma BDNF levels (p = 0.029). Interestingly, plasma BDNF levels in the non-responder group were significantly higher than those in the remission group in the initial stage of depressive syndrome (p = 0.002). Our results show that plasma BDNF levels are associated with clinical outcomes during the treatment of depression. We suggest that plasma BDNF could potentially serve as a prognostic biomarker for depression, predicting clinical outcome.Trial RegistrationUMIN Clinical Trials Registry UMIN000006264

Ketamine and other potential glutamate antidepressants

“…Plasma BDNF levels were negatively correlated to MADRS scores following ketamine infusion but not midazolam, an active control, in another sample of treatment resistant MDD (Haile et al, 2014). This finding has previously been observed in MDD patients on standard antidepressants (Kurita et al, 2012) but another ketamine study did not observe changes in BDNF (Machado-Vieira et al, 2009b). Increased BDNF function may be explained by the results of a recent study which demonstrated that MDD patients with Val/Val BDNF allele at rs6265 (Val66Met single nucleotide polymorphism) exhibited increased antidepressant response to ketamine (Laje et al, 2012).…”

BDNF plasma levels after antidepressant treatment with sertraline and transcranial direct current stimulation: Results from a factorial, randomized, sham-controlled trial

“…In this context, BDNF baseline levels were not predictors of antidepressant response either, as observed in some pharmacological studies (Kurita et al, 2012; Tadic et al, 2011; Wolkowitz et al, 2011) but not in all (Umene-Nakano et al, 2010). Nonetheless, although BDNF meta-analyses supported the notion that depression improvement is associated with BDNF increasing, virtually all BDNF trials were not controlled; therefore it was not possible to disentangle antidepressant treatment effects from time effects and also from drug effects in platelets that store BDNF in the blood.…”

Transcranial direct current stimulation (tDCS) reverts behavioral alterations and brainstem BDNF level increase induced by neuropathic pain model: Long-lasting effect

“…In some studies, BDNF is used as a biological marker of clinical conditions such as anxiety, depression, fibromyalgia, and schizophrenia (Kurita et al, 2012;Nurjono et al, 2012). However, the relationship between BDNF levels and anxiety disorders is controversial: BDNF levels appear to be either reduced increased, or not significantly altered in patients with anxiety disorders (Bonne et al, 2011;Dell'Osso et al, 2009;Dos Santos et al, 2011;Molendijk et al, 2012;Wang et al, 2011).…”