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首页> 外文期刊>Neuron >Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice.
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Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice.

机译：神经内Abeta导致转基因小鼠中早期阿尔茨海默氏病相关的认知功能障碍的发作。

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摘要

Progressive memory loss and cognitive dysfunction are the hallmark clinical features of Alzheimer's disease (AD). Identifying the molecular triggers for the onset of AD-related cognitive decline presently requires the use of suitable animal models, such as the 3xTg-AD mice, which develop both amyloid and tangle pathology. Here, we characterize the onset of learning and memory deficits in this model. We report that 2-month-old, prepathologic mice are cognitively unimpaired. The earliest cognitive impairment manifests at 4 months as a deficit in long-term retention and correlates with the accumulation of intraneuronal Abeta in the hippocampus and amygdala. Plaque or tangle pathology is not apparent at this age, suggesting that they contribute to cognitive dysfunction at later time points. Clearance of the intraneuronal Abeta pathology by immunotherapy rescues the early cognitive deficits on a hippocampal-dependent task. Reemergence of the Abeta pathology again leads to cognitive deficits. This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunction.
机译：进行性记忆丧失和认知功能障碍是阿尔茨海默氏病（AD）的标志性临床特征。鉴定引起AD相关的认知功能减退的分子触发因素目前需要使用合适的动物模型，例如3xTg-AD小鼠，其发展淀粉样蛋白和缠结病理。在这里，我们描述了该模型中学习和记忆缺陷的发作。我们报告说，两个月大的病理前小鼠在认知上没有受损。最早的认知障碍在4个月时表现为长期保留不足，并与海马和杏仁核中神经内内Abeta的积累有关。斑块或缠结病理在该年龄尚不明显，表明它们在以后的时间点助长了认知功能障碍。通过免疫疗法清除神经内Abeta病理可挽救海马依赖性任务中的早期认知缺陷。 Abeta病理学的再次出现再次导致认知缺陷。这项研究强烈牵涉神经内Abeta认知功能障碍的发作。

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