Isolated central AD-like neuropathology resultsin the loss of efferent control of GI homeostasis via the brain–gutaxis and is characterized by the insensitivity to neurally evokedmucosal secretion, altered mucus constitution with reduced mucin content,and reduced barrier-forming capacity, potentially increasing the susceptibilityof the STZ-icv rat model of AD to GI and systemic inflammation inducedby intraluminal toxins, microorganisms, and drugs. Here, MUC5AC is linked to Alzheimer disease.