Collagenous Alzheimer amyloid plaque component impacts on the compaction of amyloid-[beta] plaques

• Published in: Acta neuropathologica communications Vol. 8; no. 1
• Main Authors: Hashimoto, Tadafumi, Fujii, Daisuke, Naka, Yasushi, Kashiwagi-Hakozaki, Mayu, Matsuo, Yuko, Matsuura, Yusuke, Wakabayashi, Tomoko, Iwatsubo, Takeshi
• Format: Journal Article
• Language: English
• Published: BioMed Central Ltd 07.12.2020
• Subjects: Advertising executives; Alzheimer's disease; Genetic engineering
• ISSN: 2051-5960; 2051-5960
• DOI: 10.1186/s40478-020-01075-5

Massive deposition of amyloid [beta] peptides (A[beta]) 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[beta] 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[beta] 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[beta] in amyloid plaques and the brain dynamics of A[beta]. Keywords: Alzheimer's disease/amyloid, [beta] peptide/CLAC/senile plaques