Effect of Milnacipran on Plasma Level of Vascular Endothelial Growth Factor in Major Depression

Vascular endothelial growth factor (VEGF) was first presented as an inducer of vascular permeability, and subsequently, the understanding of its actions has broadened to include angiogenesis and vasculogenesis stimulation as well as its role as a promoter of neurogenesis and neuroprotective mechanisms.1 Moreover, it has been suggested that VEGF has an effect on alterations in cognitive function and behavior due to its direct neurogenic actions.2 The neurotrophic hypothesis of MDD postulates that stress induces alterations in neuroplastic pathways in brain areas accounting for emotional and cognitive processing, leading to reduced neurogenesis and hippocampal volume, predisposing to depression. In addition, VEGF-related polymorphisms identified by GWAS and risk for major depression, which novel association reveals VEGF suggesting the potential role of this molecule in major depression development which could help to promote a personalized medicine.3 Recent report demonstrated that VEGF plays a crucial role in the pathogenesis of major depression by increasing the Blood Brain Barriers permeability, and indicate that VEGF inhibition could be a potential therapeutic strategy for the major depression subtype associated with BBB dysfunction.4 Actually,5,6 reported that plasma VEGF is a useful biomarker of major depression, and plasma VEGF level predicts response to antidepressant. Recent our report demonstrated that paroxetine, a selective serotonin reuptake inhibitor, did not change plasma VEGF levels in patients with major depression (MD).