In Alzheimer’s disease (AD) models, BSYQ mitigates Aβ-induced neurotoxicity, preserves blood–brain barrier integrity, and facilitates Aβ clearance by regulating transport proteins such as P-glycoprotein, low-density lipoprotein receptor-related protein 1, and the receptor for advanced glycation end products (RAGE) (26). The gene discussed is AGER; the disease is early-onset autosomal dominant Alzheimer disease.