School of Public Health, Weifang Medical University, No. 7166, Baotong Xi Street, Weicheng District, Weifang 261053, China.
Tianjin Institute of Environmental and Operational Medicine, No. 1, Dali Road, Heping District, Tianjin 300050, China.
Cells. 2022 Sep 2;11(17):2742. doi: 10.3390/cells11172742.
Environmental noise is a common hazard in military operations. Military service members during long operations are often exposed to around-the-clock noise and suffer massive emotional and cognitive dysfunction related to an Alzheimer's disease (AD)-like neuropathology. It is essential to clarify the mechanisms underlying the effects of around-the-clock noise exposure on the central nervous system. Here, Wistar rats were continuously exposed to white noise (95 dB during the on-duty phase [8:00-16:00] and 75 dB during the off-duty phase (16:00-8:00 the next day)) for 40 days. The levels of phosphorylated tau, amyloid-β (Aβ), and neuroinflammation in the cortex and hippocampus were assessed and autophagosome (AP) aggregation was observed by transmission electron microscopy. Dyshomeostasis of autophagic flux resulting from around-the-clock noise exposure was assessed at different stages to investigate the potential pathological mechanisms. Around-the-clock noise significantly increased Aβ peptide, tau phosphorylation at Ser396 and Ser404, and neuroinflammation. Moreover, the AMPK-mTOR signaling pathway was depressed in the cortex and the hippocampus of rats exposed to around-the-clock noise. Consequently, autophagosome-lysosome fusion was deterred and resulted in AP accumulation. Our results indicate that around-the-clock noise exposure has detrimental influences on autophagic flux homeostasis and may be associated with AD-like neuropathology in the cortex and the hippocampus.
环境噪声是军事行动中的一种常见危害。长时间执行任务的军人经常暴露在全天候的噪声中,并因类似阿尔茨海默病(AD)的神经病理学而遭受严重的情绪和认知功能障碍。阐明全天候噪声暴露对中枢神经系统影响的机制至关重要。在这里,Wistar 大鼠连续 40 天暴露于白噪声(工作时间[8:00-16:00]为 95 dB,休息时间[16:00-8:00 次日]为 75 dB)。评估皮质和海马体中磷酸化tau、淀粉样β(Aβ)和神经炎症的水平,并通过透射电子显微镜观察自噬体(AP)聚集。在不同阶段评估全天候噪声暴露引起的自噬通量的失衡,以研究潜在的病理机制。全天候噪声显著增加了 Aβ肽、tau 在 Ser396 和 Ser404 处的磷酸化以及神经炎症。此外,暴露于全天候噪声的大鼠皮质和海马体中的 AMPK-mTOR 信号通路受到抑制。因此,自噬体-溶酶体融合受阻,导致 AP 积累。我们的结果表明,全天候噪声暴露对自噬通量平衡有不利影响,可能与皮质和海马体中的 AD 样神经病理学有关。