This hypothesis can be tested including but not limited to: (1) establishing an MC903-induced AD animal model followed by long-term (≥6 months) follow-up observations to determine whether spontaneous autoimmune manifestations develop; (2) employing organoid co-culture systems to simulate epithelial-immune cell interactions; and (3) utilizing humanized mouse models to investigate the role of alarmins such as IL-33 (54, 70–72). This evidence concerns the gene IL33 and Alzheimer disease.