Studies of pathology and pharmacology of diabetic encephalopathy with KK‐Ay mouse model

• DOI: 10.1111/cns.13201
• Publication Date: 2019-08-11T10:18:55Z
• Authors: Si Shi; Hua‐Jing Yin; Jiang Li; Ling Wang; Wei‐Ping Wang; Xiao‐Liang Wang
• Keywords: Astrogliosis; GLUT3; NeuN

Abstract Aims Pathogenesis of diabetic encephalopathy (DE) is not completely understood until now. The purposes this study were to illustrate the changes in morphology, function, and important transporters neurons glia during DE, as well reveal potential therapeutic effects medicines diet control on DE. Methods Spontaneous obese KK‐Ay mice used investigate diabetes‐induced cognitive disorder, protein expression impact animal cell level studies. new drug candidate PHPB, donepezil, low‐fat food observe effects. Results at 5 months age showed typical characteristics type 2 diabetes mellitus (T2DM） appeared significant deficits. Morphological microtubule‐associated (MAP2) was increased hippocampal glial fibrillary acidic (GFAP) decreased astrocytes. Meanwhile, vesicular glutamate transporter 1 (vGLUT1) glucose (GLUT1) decreased, brain‐derived neurotrophic factor (BDNF) cell‐derived (GDNF) also reduced mice. Microglia activated, IL‐1β TNF‐α obviously brains Most above could be relieved by intervention (DR) or treatment donepezil PHPB. Conclusion mouse a useful model for studying alterations structure, function astrocyte microglia might rescued DR medicine. proteins we reported biomarkers targets DE treatment.