Likely sources of enhanced OS in the AD brain include production of reactive oxygen species (ROS) by senescent mitochondria, accelerated β-amyloid deposition [10], elaboration of tumor necrosis factor-α (TNFα), interleukin-1 β (IL-1β) and nitric oxide (NO) by activated microglia [11] and excessive sequestration of non-transferrin iron in the diseased neural tissues [12,13]. This evidence concerns the gene TNF and Alzheimer disease.