Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Feb 15;83(4):358-368.
doi: 10.1016/j.biopsych.2017.11.020. Epub 2017 Nov 21.

Prion Protein as a Toxic Acceptor of Amyloid-β Oligomers

Silvia A Purro  1 , Andrew J Nicoll  2 , John Collinge  3
Affiliations
Review

Prion Protein as a Toxic Acceptor of Amyloid-β Oligomers

Silvia A Purro et al. Biol Psychiatry. .

Abstract

The initial report that cellular prion protein (PrPC) mediates toxicity of amyloid-β species linked to Alzheimer's disease was initially treated with scepticism, but growing evidence supports this claim. That there is a high-affinity interaction is now clear, and its molecular basis is being unraveled, while recent studies have identified possible downstream toxic mechanisms. Determination of the clinical significance of such interactions between PrPC and disease-associated amyloid-β species will require experimental medicine studies in humans. Trials of compounds that inhibit PrP-dependent amyloid-β toxicity are commencing in humans, and although it is clear that only a fraction of Alzheimer's disease toxicity could be governed by PrPC, a partial, but still therapeutically useful, role in human disease may soon be testable.

Keywords: Alzheimer’s disease; Amyloid; Neurodegeneration; Oligomers; Prion; Therapeutics.

PubMed Disclaimer

Comment in

Publication types