In line with this view, other studies performed on SAMP8 and AβPP/PS1 transgenic AD mouse models observed the accumulation of intestinal Aβ and amyloid precursor protein, enteric inflammation, mitochondrial dysfunction along with enteric glial activation and gut dysbiosis in the early stages of AD before the full development of brain pathology (Joachim et al., 1989; Puig et al., 2015; Piccarducci et al., 2019; Pellegrini et al., 2020). The gene discussed is APP; the disease is Alzheimer disease.