Amyloid beta and diabetic pathology cooperatively stimulate cytokine expression in an Alzheimer's mouse model.

ABSTRACT: BACKGROUND:Diabetes is a risk factor for developing Alzheimer's disease (AD); however, the mechanism by which diabetes can promote AD pathology remains unknown. Diabetes results in diverse molecular changes in the brain, including dysregulation of glucose metabolism and loss of cerebrovascular homeostasis. Although these changes have been associated with increased Aβ pathology and increased expression of glial activation markers in APPswe/PS1dE9 (APP/PS1) mice, there has been limited characterization, to date, of the neuroinflammatory changes associated with diabetic conditions. METHODS:To more fully elucidate neuroinflammatory changes associated with diabetes that may drive AD pathology, we combined the APP/PS1 mouse model with either high-fat diet (HFD, a model of pre-diabetes), the gene

SUBMITTER: Sankar SB 

PROVIDER: S-EPMC6988295 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature