It is not clear how the AD pathology starts, but the “spreading hypothesis” (Walsh and Selkoe, 2016) suggests that toxic mutated prion-like proteins (such as alpha-synuclein or β-amyloid or mutated tau) are consumed, taken up by the gut, and transported along the vagus nerve into the brainstem (Wang et al., 2019). The gene discussed is SNCA; the disease is Alzheimer disease.