Effects of Antidepressant Treatment on Neurotrophic Factors (BDNF and IGF-1) in Patients with Major Depressive Disorder (MDD).

Anna Mosiołek,Agata Szulc,Sławomir Jakima,Aleksandra Pięta,Jadwiga Mosiołek

doi:10.3390/jcm10153377

Abstract

Major depressive disorder (MDD) remains the subject of ongoing research as a multifactorial disease and a serious public health problem. There is a growing body of literature focusing on the role of neurotrophic factors in pathophysiology of MDD. A neurotrophic hypothesis of depression proposes that abnormalities of neurotrophins serum levels lead to neuronal atrophy and decreased neurogenesis, resulting in mood disorders. Consequently, in accordance with recent findings, antidepressant treatment modifies the serum levels of neurotrophins and thus leads to a clinical improvement of MDD. The purpose of this review is to summarize the available data on the effects of various antidepressants on serum levels of neurotrophins such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor (IGF-1). In addition, the authors discuss their role as prognostic factors for treatment response in MDD. A literature search was performed using the PubMed database. Following the inclusion and exclusion criteria, nine original articles and three meta-analyses were selected. The vast majority of studies have confirmed the effect of antidepressants on BDNF levels. Research on IGF-1 is limited and insufficient to describe the correlation between different antidepressant drugs and factor serum levels; however, four studies indicated a decrease in IGF-1 after treatment. Preliminary data suggest BDNF as a promising predictor of treatment response in MDD patients. The role of IGF-1 needs further investigation.

Highlights

Depression is the most commonly diagnosed mental disorder [1]
A possible explanation of reduced brain-derived neurotrophic factor (BDNF) in depressed patients might reflect a genetic predisposition. Another hypothesis would be that stress-induced BDNF reductions might cause neuronal damage, which would in turn lead to acquired biological vulnerability
Studies conducted on rats assessing antidepressant responses showed that conventional antidepressant drugs, as well as electroconvulsive therapy (ECT), enhanced expression of BDNF and tropomycin receptor kinase B (TrkB) mRNA in the hippocampus and cortical regions in a timeframe similar to the onset of the antidepressant-like response [52,53]

Summary

Introduction

Depression is the most commonly diagnosed mental disorder [1]. Current estimates state that around 1 in 10 individuals suffer from depression at least once in a lifetime, which would require medical treatment [2]. Depression has a multifactorial etiology, and individual hypotheses related to its formation complement each other. The updated molecular hypothesis of depression postulates that the response to antidepressants is associated with intracellular mechanisms that influence neurotrophic factors necessary for the survival and function of specific neurons [16,17]. Brain-derived neurothropic factor (BDNF) is a growth factor synthesized in the cell bodies of neurons and in glia. It affects neuronal maturation, formation of synapses and synaptic plasticity. According to the neurotrophic hypothesis of depression, the deficiency of BDNF and other growth factors may contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex, observed in patients with depression, and antidepressant drugs act by increasing the levels of BDNF [18,19,20,21,22,23]

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