Early-onset Formation of Parenchymal Plaque Amyloid Abrogates Cerebral Microvascular Amyloid Accumulation in Transgenic Mice

摘要: The fibrillar assembly and deposition of amyloid β (Aβ) protein, a key pathology Alzheimer disease, can occur in the form parenchymal plaques cerebral angiopathy (CAA). Familial forms CAA exist absence appreciable pathology. molecular interplay between is unclear. Here we investigated how early-onset impact development microvascular transgenic mice. Tg-5xFAD mice, which produce non-mutated human Aβ develop plaques, were bred to Tg-SwDI familial mutant amyloid. bigenic mice presented with an elevated accumulation brain compared either single line. Tg-SwDI/Tg-5xFAD devoid amyloid, prominent but exhibited larger deposits associated higher loss cortical neurons activated microglia periphery was largely composed Aβ. Non-mutated fibril seeds promoted formation vitro. Further, intrahippocampal administration biotin-labeled peptide accumulated on adjacent pre-existing These findings indicate that serve as scaffold capture peptides prevent their microvessels.