Seed-induced acceleration of amyloid-β mediated neurotoxicity in vivo.

ABSTRACT: Seeded propagation of amyloid-beta (Aβ) pathology is suggested to contribute to the progression of Alzheimer's disease. Local overproduction of aggregation-prone Aβ variants could explain the focal initiation of a seeding cascade that subsequently triggers widespread pathology. Several animal models support this seeding concept by demonstrating accelerated Aβ deposition following inoculation with Aβ-containing homogenates, however its role in progressive neurodegeneration remains unclear. Here, we present a non-invasive approach to study Aβ seeding processes in vivo using Drosophila models. We show that small amounts of aggregation-competent Aβ₄₂ seeds, generated in selected neuronal clusters, can induce the deposition of the pan-neuronally expressed and otherwise soluble Aβ

SUBMITTER: Sowade RF 

PROVIDER: S-EPMC5594032 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature