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.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Burdo JR,Chen Q,Calcutt NA,Schubert Ddoi
10.1016/j.neurobiolaging.2008.02.010subject
Has Abstractpub_date
2009-12-01 00:00:00pages
1910-7issue
12eissn
0197-4580issn
1558-1497pii
S0197-4580(08)00059-6journal_volume
30pub_type
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