Because of the ALAD group’s disrupted Nrf2/HO-1 axes and antioxidant status, the inflammatory cascade was triggered by increasing NF-κb expression, thereby increasing the levels of proinflammatory cytokines such as TNF-α and IL-1β, and causing neuroinflammation in AD [38,51,52]. This evidence concerns the gene HMOX1 and Alzheimer disease.