Abstract

ObjectivesBrain-derived neurotrophic factor (BDNF) has been associated with the psychopathology of both major depressive disorder (MDD) and schizophrenia (SZ). However, studies focusing on the accuracy of BDNF levels to differentiate between these patients and healthy controls (HCs) have been rare.MethodsOver a discrete ten-year period, we investigated serum BDNF levels in patients with MDD or SZ and compared them to HCs.ResultsWe found serum BDNF levels in 224 samples with SZ to be lower than those in 390 HCs samples (p = 0.007), but not lower than those in the 273 samples with MDD. Male MDD patients tended to have lower BDNF levels compared to male HCs (p = 0.083). The receiver operating characteristic curve analysis demonstrated that BDNF levels were moderately accurate in differentiating male MDD patients and female patients with SZ from HCs (AUC = 0.652 and 0.623, respectively). The most adequate cut-off points for BDNF level were 5.11 ng/ml (sensitivity = 81.1%, specificity = 48.5%) and 5.88 ng/ml (sensitivity = 74.1%, specificity = 57.4%), respectively.ConclusionsOur results support that BDNF demonstrated moderate accuracy in distinguishing male patients with MDD and female patients with SZ from HCs. In the future, greater samples would be required to further confirm these results.

Highlights

  • Brain-derived neurotrophic factor (BDNF), which was first purified [1] after the nerve growth factor was discovered [2], has been found to contribute to neurogenesis and neuroplasticity

  • We found serum BDNF levels in 224 samples with SZ to be lower than those in 390 healthy controls (HCs) samples (p = 0.007), but not lower than those in the 273 samples with major depressive disorder (MDD)

  • Male MDD patients tended to have lower BDNF levels compared to male HCs (p = 0.083)

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Summary

Introduction

Brain-derived neurotrophic factor (BDNF), which was first purified [1] after the nerve growth factor was discovered [2], has been found to contribute to neurogenesis and neuroplasticity. Clinical imaging research has supported that the flawed function and diminished volume of these neurons may be associated with depression and has revealed a dwindling size of specific brain areas. These discoveries provided the foundation for an innovative molecular and cellular hypothesis of depression. Kuhn, a physicist and science historian, previously observed that, at any given time, researchers in a specific field are inclined to hold similar basic hypotheses about their topic of study [7] This phenomena rapidly occurred for the neurotrophic hypothesis, which, since its initial proposal, was promptly extended to cover schizophrenia (SZ) by Toyooka in 2002 [8]

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