Human-like rodent amyloid-β-peptide determines Alzheimer pathology in aged wild-type Octodon degu
Human-like rodent amyloid-β-peptide determines Alzheimer pathology in aged wild-type Octodon degu
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DOI：
10.1016/j.neurobiolaging.2004.09.016
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发表时间：
2005-07-01
影响因子：
4.2
通讯作者：
Aboitiz, F
中科院分区：
文献类型：
--
作者：
Inestrosa, NC;Reyes, AE;Aboitiz, F
人们普遍认为，人类阿尔茨海默病（AD）的神经病理学标志物在啮齿动物的大脑中完全不存在。我们在这里报道了一种年老的野生型南美啮齿动物，章鱼，表达神经元β -淀粉样蛋白前体蛋白（β - app695），显示细胞内和细胞外淀粉样蛋白- β肽（A β）的沉积，细胞内tau蛋白和泛素的积累，强烈的星形细胞反应和富含乙酰胆碱酯酶（AChE）的锥体神经元。deguA β与人a β序列的高氨基酸同源性（97.5%）可能是该老年啮齿动物出现AD标记的主要因素。我们的研究结果表明，年龄为0。degu是第一个与AD相关的神经退行性过程的野生型啮齿动物模型。(c) 2004 Elsevier Inc.版权所有。
It is generally accepted that human Alzheimer's disease (AD) neuropathology markers are completely absent in rodent brains. We report here that an aged wild-type South American rodent, Octodon degu, expresses neuronal beta-amyloid precursor protein (beta-APP695) displaying both intracellular and extracellular deposits of amyloid-beta-peptide (A beta), intracellular accumulations of tau-protein and ubiquitin, a strong astrocytic response and acetylcholinesterase (AChE)-rich pyramidal neurons. The high amino acid homology (97.5%) between deguA beta and humanA beta sequences is probably a major factor in the appearance of AD markers in this aged rodent. Our results indicate that aged 0. degu constitutes the first wild-type rodent model for neurodegenerative processes associated to AD. (c) 2004 Elsevier Inc. All rights reserved.