Collagenous Alzheimer amyloid plaque component impacts on the compaction of amyloid-? plaques.

ABSTRACT: Massive deposition of amyloid ? peptides (A?) as senile plaques (SP) characterizes the brain pathology of Alzheimer's disease (AD). SPs exhibit a variety of morphologies, although little is known about the SP components that determine their morphology. Collagenous Alzheimer amyloid plaque component (CLAC) is one of the major non-A? proteinaceous components of SP amyloid in AD brains. Here we show that overexpression of CLAC precursor (CLAC-P) in the brains of APP transgenic mice results in a significant remodeling of amyloid pathology, i.e., reduction in diffuse-type amyloid plaques and an increase in compact plaques laden with thioflavin S-positive amyloid cores. In vivo microdialysis revealed a significant decrease in A? in the brain interstitial fluid of CLAC-P/APP double transgenic mice compared with APP transgenic mice. These findings implicate CLAC in the compaction of A? in amyloid plaques and the brain dynamics of A?.

SUBMITTER: Hashimoto T 

PROVIDER: S-EPMC7720522 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature