In regard to LPE/PE, although the evidence might not be sufficient, suppression of PE generation has been reported to decreased Aβ accumulation (Nesic et al., 2012), suggesting that the modulations observed in the Cerad-b brains might promote the pathogenesis of AD, while one report demonstrated that LPE suppressed inflammatory changes and oxidative stress in microglial cells (Tsukahara et al., 2021), suggesting that elevation of LPE might be a compensatory change and that failure of this modulation might lead to the pathogenesis of AD from Cerad-b (Tsukahara et al., 2021). This evidence concerns the gene PPIB and Alzheimer disease.