Although the mechanism by which upstream putatively inhibits the expression of α7nAChR was beyond the scope of this study, it is notable that Aβ-α7nAChR interaction was observed in rodent experimental models that may lead to an atomic structure damage and significant reduction in α7nAChR in AD, as evidenced by Aβ enrichment in α7nAChR-abundant regions (Wang et al., 2000; Farhat and Ahmed, 2017; Hoskin et al., 2019). This evidence concerns the gene CHRNA7 and Alzheimer disease.