2020年12月
Collagenous Alzheimer amyloid plaque component impacts on the compaction of amyloid-β plaques
Acta Neuropathologica Communications
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- 巻
- 8
- 号
- 1
- 記述言語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1186/s40478-020-01075-5
© 2020, The Author(s). 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.
- リンク情報
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- DOI
- https://doi.org/10.1186/s40478-020-01075-5
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/33287899
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85097242392&origin=inward 本文へのリンクあり
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85097242392&origin=inward
- ID情報
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- DOI : 10.1186/s40478-020-01075-5
- eISSN : 2051-5960
- PubMed ID : 33287899
- SCOPUS ID : 85097242392