Indeed, there are numerous findings regarding the pathophysiology of depression, which may become new drug targets, such as abnormalities in glutamatergic neurotransmission, neuroendocrine theory, inflammation or neurotrophic conception based on the reduced expression of brain-derived neurotrophic factor (BDNF) and/or the failure of its receptor—tyrosine receptor kinase B (TrKB) [24,25,26,27]. This evidence concerns the gene BDNF and depressive symptom measurement.