In contrast, other studies have reported that long-term administration of the TLR2 inhibitor in AD mice could reduce Aβ aggregation and glial activation [26], and that TLR2 gene knockout and the blocking of the interaction between TLR2 and MyD88 could attenuate the neurotoxicity and pathological changes of AD [27, 28]. This evidence concerns the gene TLR2 and Alzheimer disease.