THRA and Alzheimer disease: Our results suggest that the increased expression of THRα and β and their genes in the brain tissue of the mice in the experimental group may also be the mechanism of the repair response in mice at the early stage of the AD model, but further evidence is needed, which is consistent with the results reported previously [34], but contrary to the results in another report [35], the most likely reason is that the hypothalamic-pituitary-thyroid axis modulates thyroid function by a negative feedback mechanism [36, 37].