期刊
BIOMOLECULES
卷 12, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/biom12030446
关键词
amyloid inhibition; endogenous proteins; transthyretin; apolipoprotein E; clusterin; BRICHOS; amyloid-beta; IAPP; alpha-synuclein
资金
- Demensfonden
- Norrlandska Hjartfonden
- Stiftelsen Olle Engkvist Byggmastare [199-0469]
- Insamlingsstiftelsen at Umea University [FS 2.1.6-2396-18]
- FAMY-Norrbotten [03/2021]
- Wallenberg centrum for molekylar medicin [Dnr FS 2.1.6-1860-18]
Examined the anti-amyloid properties of endogenous proteins, which can interfere with amyloid formation and have clinical impact, providing potential therapeutic strategies.
Amyloid formation is a pathological process associated with a wide range of degenerative disorders, including Alzheimer's disease, Parkinson's disease, and diabetes mellitus type 2. During disease progression, abnormal accumulation and deposition of proteinaceous material are accompanied by tissue degradation, inflammation, and dysfunction. Agents that can interfere with the process of amyloid formation or target already formed amyloid assemblies are consequently of therapeutic interest. In this context, a few endogenous proteins have been associated with an anti-amyloidogenic activity. Here, we review the properties of transthyretin, apolipoprotein E, clusterin, and BRICHOS protein domain which all effectively interfere with amyloid in vitro, as well as displaying a clinical impact in humans or animal models. Their involvement in the amyloid formation process is discussed, which may aid and inspire new strategies for therapeutic interventions.
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