Article
Beta-amyloid treatment of two complementary P301L tau-expressing Alzheimer's disease models reveals similar deregulated cellular processes.
Proteomics - 1 Dec 2006
David Della C, Ittner Lars M, Gehrig Peter, Nergenau Denise, Shepherd Claire, Halliday Glenda, Götz Jürgen
Abstract excerpt
Alzheimer's disease (AD) is characterized by Abeta peptide-containing plaques and tau-containing neurofibrillary tangles (NFTs). Both pathologies have been combined by crossing Abeta plaque-forming APP mutant mice with NFT-forming P301L tau mutant mice or by stereotaxically injecting beta-amyloid peptide 1-42 (Abeta42) into brains of P301L tau mutant mice. In cell culture, Abeta42 induces filamentous tau...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
