| Autor: |
Tadafumi Hashimoto, Daisuke Fujii, Yasushi Naka, Mayu Kashiwagi-Hakozaki, Yuko Matsuo, Yusuke Matsuura, Tomoko Wakabayashi, Takeshi Iwatsubo |
| Jazyk: |
angličtina |
| Rok vydání: |
2020 |
| Předmět: |
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| Zdroj: |
Acta Neuropathologica Communications, Vol 8, Iss 1, Pp 1-18 (2020) |
| Druh dokumentu: |
article |
| ISSN: |
2051-5960 |
| DOI: |
10.1186/s40478-020-01075-5 |
| Popis: |
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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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