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.

中文翻译：

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朊病毒蛋白作为β-淀粉样蛋白寡聚体的毒性受体

关于细胞朊病毒蛋白 (PrPC) 介导与阿尔茨海默病相关的β淀粉样蛋白毒性的初步报告最初受到怀疑，但越来越多的证据支持这一说法。现在很清楚存在高亲和力相互作用，其分子基础正在被解开，而最近的研究已经确定了可能的下游毒性机制。确定 PrPC 与疾病相关的淀粉样蛋白-β 物种之间这种相互作用的临床意义将需要在人类中进行实验医学研究。抑制 PrP 依赖性淀粉样蛋白-β 毒性的化合物的试验正在人类中开始，虽然很明显只有一小部分阿尔茨海默病毒性可以由 PrPC 控制，但在人类疾病中的部分但仍具有治疗用途的作用可能很快可测试。