The above metabolic changes together determine the cognitive dysfunction in diabetic rats, and our study supports the hypothesis previously proposed, namely that changes in brain Aβ42, P-tau protein, IL-6, and ACh expression are the early events in diabetic memory impairment, and the latency period of the latter may provide an intervention time window for preventing cognitive impairment in DM. The gene discussed is IL6; the disease is Cognitive impairment.