Bayer Thomas A, Breyhan Henning, Duan Kailai, Rettig Jens, Wirths Oliver
Department of Psychiatry, Division of Molecular Psychiatry, University of Goettingen, Goettingen, Germany.
Neurodegener Dis. 2008;5(3-4):140-2. doi: 10.1159/000113684. Epub 2008 Mar 6.
Accumulating evidence points to an important role of intraneuronal beta-amyloid (Abeta) in the development of Alzheimer's disease (AD), with its typical clinical symptoms like memory impairment and changes in personality. We have previously reported on the Abeta precursor protein and presenilin-1 knock-out (APP/PS1KI) mouse model with abundant intraneuronal Abeta(42) accumulation and a 50% loss of CA1 neurons at 10 months of age. In addition, we observed reduced short- and long-term synaptic plasticity, hippocampal neuron loss, and reduced performance in a working memory task. These observations support a pivotal role of intraneuronal Abeta accumulation as a principal pathological trigger in AD.
越来越多的证据表明，神经元内β-淀粉样蛋白（Aβ）在阿尔茨海默病（AD）的发展中起重要作用，AD具有记忆障碍和性格改变等典型临床症状。我们之前报道过Aβ前体蛋白和早老素1基因敲除（APP/PS1KI）小鼠模型，该模型在10月龄时神经元内有大量Aβ（42）积累，且CA1神经元损失50%。此外，我们观察到短期和长期突触可塑性降低、海马神经元丢失以及工作记忆任务中的表现下降。这些观察结果支持神经元内Aβ积累作为AD主要病理触发因素的关键作用。
