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首页> 外文期刊>Neurobiology of Aging: Experimental and Clinical Research >Age-dependent axonal degeneration in an Alzheimer mouse model.
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Age-dependent axonal degeneration in an Alzheimer mouse model.

机译：老年性痴呆小鼠模型中年龄依赖性的轴突变性。

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Some neurodegenerative diseases including Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS) exhibit prominent defects in axonal transport. These defects can manifest as axonal swellings or spheroids, which correspond to axonal enlargements and aberrant accumulation of axonal cargoes, cytoskeletal proteins and lipids. Recently, a controversial scientific debate focussed on the issue whether Abeta serves as a trigger for aberrant axonal transport in the pathophysiology of AD. Prominent axonopathy has been shown to be induced by overexpression of proteins involved in several neurodegenerative diseases. Neurofilament, apolipoprotein E, Niemann-Pick protein and Tau transgenic mice with axonal trafficking deficits have been reported. Furthermore, motor deficits are frequently observed in patients with AD, which has been attributed to the typical tauopathy in post-mortem brain tissue. In the present report, we analyzed axonal neuropathology in the brain and spinal cord of a transgenic mouse model with abundant intraneuronal Abeta42 production and provide compelling evidence for axonal degeneration. The APP/PS1ki mice showed characteristic axonal swellings, spheroids, axonal demyelination and ovoids, which are myelin remnants of degenerated nerve fibers in an age-dependent manner. Abundant accumulation of intraneuronal N-modified Abeta, Thioflavin S-positive material and ubiquitin was found within the somatodendritic compartment of neurons. We conclude that the intraneuronal accumulation of Abeta-amyloid peptides is followed by axonal degeneration, and thus might be a causative factor for the axonal changes seen in AD.
机译：一些神经退行性疾病，包括阿尔茨海默氏病（AD）和肌萎缩性侧索硬化症（ALS），在轴突运输中表现出明显的缺陷。这些缺陷可表现为轴突肿胀或球状，对应于轴突肿大和轴突货物，细胞骨架蛋白和脂质的异常积累。最近，一个有争议的科学辩论集中在Abeta是否在AD的病理生理学中充当异常轴突运输的触发因素的问题上。已经显示出突出的轴突病是由与几种神经退行性疾病有关的蛋白质的过表达诱导的。已经报道了具有轴突运输缺陷的神经丝，载脂蛋白E，Niemann-Pick蛋白和Tau转基因小鼠。此外，在AD患者中经常观察到运动缺陷，这归因于死后脑组织中典型的tauopathy。在本报告中，我们分析了具有大量神经元内Abeta42产生的转基因小鼠模型的大脑和脊髓中的轴突神经病理学，并为轴突变性提供了有力的证据。 APP / PS1ki小鼠表现出特征性的轴突肿胀，球体，轴突脱髓鞘和卵圆形，它们是变性神经纤维的髓磷脂残留物，并具有年龄依赖性。在神经元的体树突状区室中发现了神经元内N修饰的Abeta，硫黄素S阳性物质和泛素的大量积累。我们得出的结论是，Aβ-淀粉样蛋白肽在神经内积聚之后是轴突变性，因此可能是AD中轴突变化的原因。

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