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• W2044505913 endingPage "1917" @default.
• W2044505913 startingPage "1910" @default.
• W2044505913 abstract "Since diabetes is a risk factor for Alzheimer's disease (AD), we asked if there is a functional interaction between high glucose and elevated beta amyloid peptide (Abeta) in cultured brain microvascular endothelial cells and presymptomatic AD transgenic mice. When cultured brain microvascular endothelial cells are exposed to both high glucose and low levels of Abeta, there is a synergistic interaction to cause an increased accumulation of advanced glycation products (AGE) and reactive oxygen species (ROS). When presymptomatic mice expressing mutant human amyloid precursor protein and presenilin are made diabetic, they have a decrease in cognitive function relative to control mice. Associated with the cognitive deficit are increases in brain microvascular AGE and iNOS expression, and the loss of the synaptic spine protein drebrin. No amyloid plaques or tangles are observed within the brains of any group. These data show that diabetes causes a synergistic potentiation of some indices of AD in transgenic animals that are presymptomatic for the classical features of the disease." @default.
• W2044505913 created "2016-06-24" @default.
• W2044505913 creator A5014708668 @default.
• W2044505913 creator A5024725992 @default.
• W2044505913 creator A5025416818 @default.
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• W2044505913 date "2009-12-01" @default.
• W2044505913 modified "2023-10-14" @default.
• W2044505913 title "The pathological interaction between diabetes and presymptomatic Alzheimer's disease" @default.
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• W2044505913 doi "https://doi.org/10.1016/j.neurobiolaging.2008.02.010" @default.
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