At the cellular and molecular levels, the underlying mechanisms that mediate the pathogenesis of depression-like neuropathology involve an exaggerated oxidative/nitrosative stress and excessive production of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL-1β) in several brain regions, including the hippocampus [2,3,5,6]. This evidence concerns the gene TNF and depressive symptom measurement.