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• W2045600195 startingPage "11165" @default.
• W2045600195 abstract "The roles of oxidative stress and structural alterations in the cerebrovascular dysfunctions associated with Alzheimer's disease (AD) were investigated in transgenic mice overexpressing amyloid precusor protein (APP + ) or transforming growth factor-β1 (TGF + ). Age-related impairments and their in vitro reversibility were evaluated, and underlying pathogenic mechanisms were assessed and compared with those seen in AD brains. Vasoconstrictions to 5-HT and endothelin-1 were preserved, except in the oldest (18-21 months of age) TGF + mice. Despite unaltered relaxations to sodium nitroprusside, acetylcholine (ACh) and calcitonin gene-related peptide-mediated dilatations were impaired, and there was an age-related deficit in the basal availability of nitric oxide (NO) that progressed more gradually in TGF + mice. The expression and progression of these deficits were unrelated to the onset or extent of thioflavin-S-positive vessels. Manganese superoxide dismutase (SOD2) was upregulated in pial vessels and around brain microvessels of APP + mice, pointing to a role of superoxide in the dysfunctions elicited by amyloidosis. In contrast, vascular wall remodeling associated with decreased levels of endothelial NO synthase and cyclooxygenase-2 and increased contents of vascular endothelial growth factor and collagen-I and -IV characterized TGF + mice. Exogenous SOD or catalase normalized ACh dilatations and NO availability in vessels from aged APP + mice but had no effect in those of TGF + mice. Increased perivascular oxidative stress was not evidenced in AD brains, but vascular wall alterations compared well with those seen in TGF + mice. We conclude that brain vessel remodeling and associated alterations in levels of vasoactive signaling molecules are key contributors to AD cerebrovascular dysfunctions." @default.
• W2045600195 created "2016-06-24" @default.
• W2045600195 creator A5034286359 @default.
• W2045600195 creator A5054853779 @default.
• W2045600195 creator A5063552156 @default.
• W2045600195 creator A5083183405 @default.
• W2045600195 date "2005-11-30" @default.
• W2045600195 modified "2023-10-15" @default.
• W2045600195 title "Vascular Remodeling versus Amyloid β-Induced Oxidative Stress in the Cerebrovascular Dysfunctions Associated with Alzheimer's Disease" @default.
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• W2045600195 doi "https://doi.org/10.1523/jneurosci.4031-05.2005" @default.
• W2045600195 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6725645" @default.
• W2045600195 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16319316" @default.
• W2045600195 hasPublicationYear "2005" @default.

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