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评估交通相关空气污染引起的纤维特异性白质退化与老年大鼠运动性能下降的关系。

Assessing traffic-related air pollution-induced fiber-specific white matter degradation associated with motor performance declines in aged rats.

机构信息

Department of Biomedical Engineering, National Yang Ming Chiao Tung University, 155 Linong St., Section 2, Taipei 11221, Taiwan.

Ph.D. Program in Medical Neuroscience, Taipei Medical University, Taipei Medical University, No. 250 Wu-Xing St., Taipei 11031, Taiwan.

出版信息

Ecotoxicol Environ Saf. 2023 Sep 15;263:115373. doi: 10.1016/j.ecoenv.2023.115373. Epub 2023 Aug 22.

Abstract

Fine particulate matter (PM) is thought to exacerbate Parkinson's disease (PD) in the elderly, and early detection of PD progression may prevent further irreversible damage. Therefore, we used diffusion tensor imaging (DTI) for probing microstructural changes after late-life chronic traffic-related PM exposure. Herein, 1.5-year-old Fischer 344 rats were exposed to clean air (control), high-efficiency particulate air (HEPA)-filtered ambient air (HEPA group), and ambient traffic-related PM (PM group, 9.933 ± 1.021 µg/m) for 3 months. Rotarod test, DTI tractographic analysis, and immunohistochemistry were performed in the end of study period. Aged rats exposed to PM exhibited motor impairment with decreased fractional anisotropy and tyrosine hydroxylase expression in olfactory and nigrostriatal circuits, indicating disrupted white matter integrity and dopaminergic (DA) neuronal loss. Additionally, increased radial diffusivity and lower expression of myelin basic protein in PM group suggested ageing progression of demyelination exacerbated by PM exposure. Significant production of tumor necrosis factor-α was also observed after PM exposure, revealing potential inflammation of injury to multiple fiber tracts of DA pathways. Microstructural changes demonstrated potential links between PM-induced inflammatory white matter demyelination and behavioral performance, with indication of pre-manifestation of DTI-based biomarkers for early detection of PD progression in the elderly.

摘要

细颗粒物(PM)被认为会加重老年人的帕金森病(PD),早期发现 PD 的进展可能会防止进一步的不可逆转的损伤。因此,我们使用扩散张量成像(DTI)来探测晚年慢性交通相关 PM 暴露后的微观结构变化。在这里,1.5 岁的 Fischer 344 大鼠暴露于清洁空气(对照)、高效微粒空气(HEPA)过滤的环境空气(HEPA 组)和环境交通相关的 PM(PM 组,9.933±1.021µg/m)3 个月。在研究期末进行了旋转棒试验、DTI 轨迹分析和免疫组织化学。暴露于 PM 的老年大鼠表现出运动障碍,嗅觉和黑质纹状体回路中的分数各向异性和酪氨酸羟化酶表达降低,表明白质完整性和多巴胺能(DA)神经元丧失受损。此外,PM 组的径向扩散率增加和髓鞘碱性蛋白表达降低表明 PM 暴露加剧了脱髓鞘的老化进展。PM 暴露后还观察到肿瘤坏死因子-α的大量产生,表明 PM 对 DA 通路的多条纤维束的损伤具有潜在的炎症。微观结构变化显示了 PM 诱导的炎症性白质脱髓鞘与行为表现之间的潜在联系,并表明基于 DTI 的生物标志物具有在老年人中早期检测 PD 进展的潜力。

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