细颗粒物（PM2.5）被认为加剧老年人帕金森病（PD），早期检测PD进展可能防止进一步不可逆转的损害。因此，我们使用扩散张量成像（DTI）探测晚期长期接触交通相关PM2.5后的微观结构变化。在此研究中，1.5岁的Fischer 344大鼠暴露于洁净空气（对照组），高效率除尘过滤的环境空气（HEPA组）和环境交通相关PM2.5（PM2.5组，9.933±1.021µg/m3）3个月。在研究期末进行旋转杆测试、DTI径迹分析和免疫组化学检测。暴露于PM2.5的老龄大鼠表现出运动障碍，伴随嗅觉和黑质纹状体回路的小区异性系数和酪氨酸羟化酶表达减少，表明白质完整性和多巴胺能（DA）神经元丧失受到破坏。此外，PM2.5组的径向弥散度增加和髓鞘基础蛋白表达降低暗示PM2.5暴露加剧了脱髓鞘的老化进展。PM2.5暴露后还观察到明显的肿瘤坏死因子-α产生，揭示了对多条DA通路纤维损伤的潜在炎症。微观结构变化显示PM2.5诱导的炎症性白质脱髓鞘与行为表现之间存在潜在联系，并提示DTI基础生物标志物可能用于早期检测老年人PD进展的预显症。版权所有 © 2023 作者。由Elsevier Inc.发表 归该作者版权所有。

Fine particulate matter (PM2.5) 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 PM2.5 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 PM2.5 (PM2.5 group, 9.933 ± 1.021 µg/m3) for 3 months. Rotarod test, DTI tractographic analysis, and immunohistochemistry were performed in the end of study period. Aged rats exposed to PM2.5 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 PM2.5 group suggested ageing progression of demyelination exacerbated by PM2.5 exposure. Significant production of tumor necrosis factor-α was also observed after PM2.5 exposure, revealing potential inflammation of injury to multiple fiber tracts of DA pathways. Microstructural changes demonstrated potential links between PM2.5-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.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.