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

Si Shi1, Hua-Jing Yin1, Jiang Li1

  • 1Department of Pharmacology, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

CNS Neuroscience & Therapeutics
|August 12, 2019
PubMed
Abstract

Insights

Diabetic encephalopathy (DE) in KK-Ay mice shows cognitive decline and altered brain cell function. Diet and medications like PHPB and donepezil may reverse these changes, offering potential therapeutic targets.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Diabetic encephalopathy (DE) pathogenesis remains unclear.
  • Understanding DE's impact on neuronal and glial cells is crucial.
  • Identifying therapeutic strategies for DE is a priority.

Purpose of the Study:

  • To investigate morphological and functional changes in neurons and glia during DE.
  • To identify key transporters affected in DE.
  • To evaluate the therapeutic potential of medications and diet in DE.

Main Methods:

  • Utilized spontaneous obese KK-Ay mice as a model for type 2 diabetes mellitus (T2DM) and cognitive deficits.
  • Performed morphological and protein expression studies at the animal and cellular levels.
  • Assessed therapeutic effects of a new drug candidate (PHPB), donepezil, and dietary intervention (DR).

Main Results:

  • KK-Ay mice exhibited significant cognitive deficits, altered MAP2, GFAP, vGLUT1, and GLUT1 expression.
  • Reduced BDNF and GDNF levels, activated microglia, and increased IL-1β and TNF-α were observed.
  • Dietary intervention (DR) and treatments with PHPB or donepezil ameliorated these DE-related changes.

Conclusions:

  • KK-Ay mice serve as a valuable model for studying DE.
  • Dietary intervention and specific medications can rescue DE-induced alterations in astrocytes and microglia.
  • Identified proteins may serve as biomarkers and potential therapeutic targets for DE.
Keywords:
GFAPKK-AyMAP2PHPBdiabetic encephalopathy

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