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期刊来源：Nat Med

原文链接：https://doi.org/10.1038/s41591-023-02729-2

摘要内容如下：

阿尔茨海默病（AD）的病理特征是脑实质和血管中的β淀粉样蛋白（Aβ）沉积（如大脑淀粉样血管病（CAA））和过度磷酸化tau蛋白的神经原纤维缠结。令人信服的遗传和生物标志物证据支持Aβ是AD的根本原因。我们先前报道了Aβ病理和CAA在相对年轻的成年人中的人类传播，这些人在儿童期使用被CJD朊病毒和Aβ种子污染的尸体来源垂体生长激素（C-hGH）治疗后死于医源性克雅氏病（ICJD）。这增加了没有死于ICJD的C-hGH接受者最终发展为AD的可能性。在这里，我们描述了在AD的表型谱中发生痴呆和生物标志物变化的接受者，这表明AD与CJD一样，具有环境获得性（医源性）形式以及晚发性散发性和早发性遗传性形式。尽管医源性AD可能很罕见，并且没有迹象表明Aβ可以在日常生活活动中在个体之间传播，但对它的认识强调了需要审查措施，以防止通过其他医疗和外科手术意外传播。由于传播的Aβ组装体可能表现出类似于常规朊病毒的结构多样性，因此针对疾病相关组装体的治疗策略可能导致次要成分的选择和耐药性的产生。

英文原文如下：

Abstracts

Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau. Compelling genetic and biomarker evidence supports Aβ as the root cause of AD. We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt-Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds. This raised the possibility that c-hGH recipients who did not die from iCJD may eventually develop AD. Here we describe recipients who developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms. Although iatrogenic AD may be rare, and there is no suggestion that Aβ can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures. As propagating Aβ assemblies may exhibit structural diversity akin to conventional prions, it is possible that therapeutic strategies targeting disease-related assemblies may lead to selection of minor components and development of resistance.

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