At present, studies have documented that TNF-α monoclonal antibodies can reduce Aβ plaque formation and alleviate the symptoms of AD (Shi et al., 2011) and that a long-term use of nonsteroidal anti-inflammatory drugs can inhibit AD progression (McGeer et al., 1996; Anthony et al., 2000), implying that a targeted reduction of neuroinflammation is indeed effective in alleviating the progression of AD. This evidence concerns the gene TNF and Alzheimer disease.