| First Author | Steinhoff T | Year | 2001 |
| Journal | Neurobiol Dis | Volume | 8 |
| Issue | 4 | Pages | 647-54 |
| PubMed ID | 11493029 | Mgi Jnum | J:71189 |
| Mgi Id | MGI:2149280 | Doi | 10.1006/nbdi.2001.0412 |
| Citation | Steinhoff T, et al. (2001) Increased cystatin C in astrocytes of transgenic mice expressing the K670N-M671L mutation of the amyloid precursor protein and deposition in brain amyloid plaques. Neurobiol Dis 8(4):647-54 |
| abstractText | 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. |
