The pathophysiology of depression encompasses multiple hypotheses (Li et al., 2021), including: Monoamine hypothesis (Dysregulation of serotonin, norepinephrine, and dopamine); HPA axis dysfunction (Hyperactivity in stress-response pathways); Glutamatergic signaling (Excitotoxicity and synaptic plasticity deficits); GABAergic inhibition (Reduced GABA neurotransmission); Neurotrophic factors: (Impaired brain-derived neurotrophic factor signaling); Neuroinflammation (Elevated pro-inflammatory cytokines). The gene discussed is BDNF; the disease is depressive symptom measurement.