IL1B and depressive symptom measurement: Neurochemical imbalances and impaired synaptic plasticity, biological mechanisms linked to the pathophysiology of depression, may be exacerbated by impairments of glial cells, including astrocytes and changes in inflammatory markers, such as IL-1β, which induces mesencephalic progenitor cells in rats to transform into a dopaminergic phenotype, and IL-6, which decreases the survival of serotonergic neurons in the fetal brain [4,5,6].