Molecular Regulation and Therapeutic Applications of Brain-Derived Neurotrophic Factor–Tropomyosin-Related Kinase B Signaling in Major Depressive Disorder Though Its Interaction with Vascular Endothelial Growth Factor and N-Methyl-D-Aspartic Acid Receptors: A Narrative Review

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The molecular regulation and therapeutic applications of brain-derived neurotrophic factor (BDNF)–tropomyosin-related kinase B (TrkB) signaling in major depressive disorder (MDD) through interaction with vascular endothelial growth factor (VEGF) and N-methyl-D-aspartic acid (NMDA) receptors show promise. While BDNF-TrkB signaling is implicated in antidepressant action, the association between BDNFs and depression has not yielded conclusive results. Some studies show decreased BDNF levels in depression, while others indicate that increased BDNF expression in certain brain regions can induce depression susceptibility. The role of BDNFs varies across different brain regions, necessitating further study of individual mechanisms. This regional variability complicates the development of targeted therapies. The antidepressant-like and neurotrophic actions of BDNFs require VEGF signaling, but there is also a reciprocal interdependence, as VEGF actions are dependent on BDNFs. This complex relationship complicates the development of targeted therapies.