Prion-like induction of Alzheimer-type proteopathy in transgenic animals

摘要

Both Alzheimer's disease and prion disease involve the accumulation of specific proteins in the brain, suggesting pathogenic commonalities. In Alzheimer's disease, the aggregation of the protein fragment Aβ is a seminal event. Similar to the templated corruption of prion protein, cerebral Aβ deposition can be induced in human β-amyloid precursor protein (APP)-transgenic rodents by the intracerebral injection of Aβ-rich brain extracts from patients with Alzheimer's disease, aged monkeys, or from APP-transgenic mice. The characteristics of the seeded deposits depend on the source of the seeding extract, the type of host, and the seeded brain region. Experimental evidence indicates that misfolded Aβ is an essential component of the seed. Acknowledgments: Supported by NIH RR-00165, P50AG025688 and the CART Foundation.