Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease.

ABSTRACT:

Background

The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease. The prediction has been that reducing Abeta production in the brain, even after the onset of clinical symptoms and the development of associated pathology, will facilitate the repair of damaged tissue and removal of amyloid lesions. However, no long-term studies using animal models of amyloid pathology have yet been performed to test this hypothesis.

Methods and findings

We have generated a transgenic mouse model that genetically mimics the arrest of Abeta production expected from treatment with secretase inhibitors. These mice overexpress mutant APP fr

SUBMITTER: Jankowsky JL 

PROVIDER: S-EPMC1283364 | biostudies-literature | 2005 Dec

REPOSITORIES: biostudies-literature