Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA.
Acta Neuropathol Commun. 2013 Nov 18;1(1):76. doi: 10.1186/2051-5960-1-76.
One of the main features of Alzheimer's disease (AD) is the presence of Aβ deposits, which accumulate in the brain years before the onset of symptoms. We and others have demonstrated that cerebral Aβ-amyloidosis can be induced in vivo by administration of AD-brain extracts into transgenic mice. However, it is currently unknown whether amyloid formation can be induced using extracts from individuals harboring Aβ deposits, but not clinical disease.
In this study we analyzed the amyloid-inducing capability of samples from individuals affected by mild cognitive impairment (MCI) and Non-Demented persons with Alzheimer's disease Neuropathology (NDAN). Our results show that inoculation of transgenic mice with MCI and NDAN brain samples accelerated Aβ pathology in a similar way as extracts from confirmed AD.
This data demonstrate that the sole presence of Aβ aggregates in a given sample, regardless of the clinical condition, is capable to accelerate Aβ deposition in vivo. These findings indicate that the amyloid-inducing activity may be present in the brain of people during pre-symptomatic or a-symptomatic stages of AD.
阿尔茨海默病（AD）的主要特征之一是存在 Aβ 沉积，这些沉积在症状出现前多年就在大脑中积累。我们和其他人已经证明，通过向转基因小鼠中给予 AD 脑提取物，可以在体内诱导脑 Aβ-淀粉样蛋白病。然而，目前尚不清楚是否可以使用仅存在 Aβ 沉积但没有临床疾病的个体的提取物来诱导淀粉样蛋白形成。
在这项研究中，我们分析了来自轻度认知障碍（MCI）和非痴呆阿尔茨海默病神经病理学（NDAN）个体的样本的淀粉样蛋白诱导能力。我们的结果表明，用 MCI 和 NDAN 脑样本接种转基因小鼠可加速 Aβ 病理学，其方式与确认的 AD 提取物相似。
这些数据表明，仅存在给定样本中的 Aβ 聚集物，无论临床状况如何，都能够在体内加速 Aβ 沉积。这些发现表明，在 AD 的无症状或症状前阶段，人的大脑中可能存在淀粉样蛋白诱导活性。
