Prion Protein as a Toxic Acceptor of Amyloid-β Oligomers

被引：60

作者：

Purro, Silvia A. ^{[1
]}

Nicoll, Andrew J. ^{[1
,2
]}

Collinge, John ^{[1
]}

机构：

[1] UCL, Inst Prion Dis, MRC, Prion Unit, London, England

[2] Elkington & Fife LLP, London, Kent, England

来源：

BIOLOGICAL PSYCHIATRY | 2018年 / 83卷 / 04期

基金：

英国医学研究理事会;

关键词：

Alzheimer's disease; Amyloid; Neurodegeneration; Oligomers; Prion; Therapeutics; ALZHEIMERS-DISEASE BRAIN; GLUTAMATE-RECEPTOR; 5; N-TERMINAL FRAGMENT; CELLULAR PRION; A-BETA; SYNAPTIC-PLASTICITY; IN-VIVO; MEMORY IMPAIRMENT; TRANSGENIC MICE; NEURODEGENERATIVE DISEASES;

D O I：

10.1016/j.biopsych.2017.11.020

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The initial report that cellular prion protein (PrPC) mediates toxicity of amyloid-beta 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-beta species will require experimental medicine studies in humans. Trials of compounds that inhibit PrP-dependent amyloid-beta 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.

引用

页码：358 / 368

页数：11

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