Concerns are growing that exposure to environmental pollutants, such as traffic noise, might cause cognitive impairments and predispose individuals toward the development of Alzheimer's disease (AD) dementia. In this study in a knock‐in mouse model of AD, we investigated how chronic traffic noise exposure (CTNE) impacts cognitive performance and amyloid‐beta (Aβ) pathology. A group of APP^{NL‐G‐F/NL‐G‐F} mice was exposed to CTNE (70 dB_A, 8 hr/day for 1 month) and compared with nonexposed counterparts. Following CTNE, an increase in hypothalamic–pituitary–adrenal (HPA) axis responsivity was observed by corticosterone assay of the blood. One month after CTNE, the CTNE group demonstrated impairments in cognitive and motor functions, and indications of anxiety‐like behavior, relative to the control animals. The noise‐exposed group also showed elevated Aβ aggregation, as inferred by a greater number of plaques and larger average plaque size in various regions of the brain, including regions involved in stress regulation. The results support that noise‐associated dysregulation of the neuroendocrine system as a potential risk factor for developing cognitive impairment and Aβ pathology, which should be further investigated in human studies.

中文翻译：

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AD 小鼠模型中的交通噪声暴露、认知能力下降和β-淀粉样蛋白病理学

人们越来越担心，暴露于交通噪音等环境污染物可能会导致认知障碍，并使个体更容易患上阿尔茨海默病 (AD) 痴呆症。在这项针对 AD 敲入小鼠模型的研究中，我们研究了慢性交通噪声暴露 (CTNE) 如何影响认知能力和淀粉样蛋白-β (Aβ) 病理学。一组 APP ^{NL-G-F/NL-G-F}小鼠暴露于 CTNE (70 dB _A，每天 8 小时，持续 1 个月）并与未暴露的对应物进行比较。CTNE 后，通过血液皮质酮测定观察到下丘脑-垂体-肾上腺 (HPA) 轴反应性增加。CTNE 后 1 个月，与对照动物相比，CTNE 组表现出认知和运动功能障碍，以及焦虑样行为的迹象。噪声暴露组也显示出 Aβ 聚集升高，这可以通过大脑不同区域（包括参与压力调节的区域）中更多的斑块和更大的平均斑块大小来推断。结果支持噪声相关的神经内分泌系统失调是发生认知障碍和 Aβ 病理学的潜在风险因素，应在人体研究中进一步研究。