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

Tadafumi Hashimoto, Daisuke Fujii, Yasushi Naka, Mayu Kashiwagi-Hakozaki, Yuko Matsuo, Yusuke Matsuura, Tomoko Wakabayashi, Takeshi Iwatsubo
2020 Acta Neuropathologica Communications  
AbstractMassive deposition of amyloid β peptides (Aβ) 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-Aβ 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
more » ... sgenic 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 Aβ 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 Aβ in amyloid plaques and the brain dynamics of Aβ.
doi:10.1186/s40478-020-01075-5 pmid:33287899 fatcat:2elnubgxqbcxvediojyo6fblla