Abstract: Objective To study the pathogenic mechanisms of diabetic encephalopathy. Methods Using KK-Ay mouse as the non-insulin dependent diabetes mellitus(NIDDM) model and age-matched C57BL/6J mouse as normal control, their cognitive performance in Morris water maze and morphological change in brain has been observed respectively at 6 and 12 weeks after onset of diabetes mellitus. Results KK-Ay diabetic mouse begin to display moderate learning deficits in the Morris maze 6 weeks after onset of diabetes. The cognitive impairment become more significant at 12 weeks: the swimming time and distance of diabetic mouse is significantly longer than the control; the pathological change of brain tissue has been observed by electron microscopy and light microscopy. Conclusion KK-Ay diabetic mouse can be used as an animal model to study the pathogenesis of diabetic encephalopathy. The hyperglycemia may lead to the cognitive impairment in diabetes.

Key words: diabetic encephalopathy, pathogenetic mechanism, KK-Ay diabetic mouse, cognitive impairment