Acta Neuropathologica Communications (Dec 2020)

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

DOI
https://doi.org/10.1186/s40478-020-01075-5
Journal volume & issue
Vol. 8, no. 1
pp. 1 – 18

Abstract

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Abstract Massive 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 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.

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