作者: Rebecca F. Rosen , Jason J. Fritz , Jeromy Dooyema , Amarallys F. Cintron , Tsuyoshi Hamaguchi
DOI: 10.1111/J.1471-4159.2011.07551.X
关键词:
摘要: J. Neurochem. (2012) 120, 660–666. Abstract Deposition of the amyloid-β (Aβ) peptide in senile plaques and cerebral Aβ angiopathy (CAA) can be stimulated Aβ-precursor protein (APP)-transgenic mice by intracerebral injection dilute brain extracts containing aggregated seeds. Growing evidence implicates a prion-like mechanism corruptive templating this phenomenon, which itself is seed. Unlike prion disease, induced de novo animals that are unlikely to spontaneously develop previous experiments with seeding have employed animal models that, as they age, eventually will generate lesions absence seeding. In present study, we first established transgenic rat model expressing human APP (APP21 line) does not manifest endogenous deposits within course its median lifespan (30 months). Next, injected 3-month-old APP21 rats intrahippocampally Alzheimer Aβ. After 9-month incubation period, these had developed CAA hippocampus, whereas control remained free such lesions. These findings underscore co-dependence agent host governing seeded aggregation, show Aβ-amyloidosis even relatively refractory spontaneous origination parenchymal vascular