Center for Biomedical Research (CIB), Faculty of Medicine, University of Cartagena, Cartagena, Colombia.
Faculty of Medicine, El Bosque University, Bogota, Colombia.
Curr Alzheimer Res. 2020;17(9):781-789. doi: 10.2174/1567205017666201204164220.
Recent studies have recognized similarities between the peptides involved in the neuropathology of Alzheimer's disease and prions. The Tau protein and the Amyloid β peptide represent the theoretical pillars of Alzheimer's disease development. It is probable that there is a shared mechanism for the transmission of these substances and the prion diseases development; this presumption is based on the presentation of several cases of individuals without risk factors who developed dementia decades after a neurosurgical procedure. This article aims to present the role of Aβ and Tau, which underlie the pathophysiologic mechanisms involved in the AD and their similarities with the prion diseases infective mechanisms by means of the presentation of the available evidence at molecular (in-vitro), animal, and human levels that support the controversy on whether these diseases might be transmitted in neurosurgical interventions, which may constitute a wide public health issue.
最近的研究已经认识到阿尔茨海默病神经病理学中涉及的肽与朊病毒之间的相似性。Tau 蛋白和淀粉样 β 肽代表了阿尔茨海默病发展的理论支柱。这些物质的传播和朊病毒疾病发展可能存在共同的机制;这种假设基于一些没有风险因素的个体在神经外科手术后几十年发展为痴呆的病例。本文旨在介绍 Aβ 和 Tau 的作用,它们是 AD 涉及的病理生理机制的基础,并通过在分子(体外)、动物和人体水平上呈现现有的证据来展示它们与朊病毒疾病感染机制的相似性,这些证据支持关于这些疾病是否可能在神经外科干预中传播的争议,这可能构成一个广泛的公共卫生问题。