To exclude the possibility that enteric network density loss was caused by APP overexpression in 5XFAD mice, we examined colon structures in APPNL-F-G knock-in (KI) mice which expressed human AD mutations at a humanized mouse APP locus; mutations were driven by the APP endogenous promoter, therefore animals developed neurocognitive defects and amyloid plaques [38]. This evidence concerns the gene APP and Alzheimer disease.