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• W2010839324 abstract "Cystatin C is an essential secretory cofactor for neurogenesis with potent protease inhibitor activities. Polymorphisms of cystatin C are genetically associated with Alzheimer's disease (AD), and the L68Q mutation causes hereditary cerebral hemorrhage with amyloidosis of the Icelandic type, in which cystatin C and beta-amyloid are colocalized in cortical blood vessels. To determine whether cystatin C and beta-amyloid also colocalize in brain amyloid plaques, we analyzed transgenic mice expressing the Swedish APP (SweAPP) mutation. We found high levels of cystatin C in astrocytes surrounding beta-amyloid plaques, and discrete layers of cystatin C attached to amyloid plaque cores covered by a layer of beta-amyloid. In addition, cystatin C accumulated in reactive astrocytes throughout the brain, independently of, and before the onset of, amyloid plaque formation. These results show that expression of SweAPP is associated with increased cystatin C in reactive astrocytes, and they suggest an early role of cystatin C in appositional amyloid plaque growth." @default.
• W2010839324 created "2016-06-24" @default.
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• W2010839324 date "2001-08-01" @default.
• W2010839324 modified "2023-10-13" @default.
• W2010839324 title "Increased Cystatin C in Astrocytes of Transgenic Mice Expressing the K670N-M671L Mutation of the Amyloid Precursor Protein and Deposition in Brain Amyloid Plaques" @default.
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• W2010839324 doi "https://doi.org/10.1006/nbdi.2001.0412" @default.
• W2010839324 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11493029" @default.
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