The current consensus is that neuroinflammation plays a pivotal role in AD progression (Wang W. Y. et al., 2015), which is supported by results from APP transgenic mouse models in which injection of lipopolysaccharide (LPS, TLR4 activator) triggers neuroinflammation with two cellular hallmarks of AD in the brain, amyloid β-protein deposition (Lee et al., 2008; Go et al., 2016) and tau hyperphosphorylation (Kitazawa et al., 2005; Lee et al., 2010). This evidence concerns the gene MAPT and Alzheimer disease.