Wang Fengxu, Wang Jin, Luo Na, Luo Yonghua, Gao Zhengnan, Cui Ye, Jiang Mengna, Shen Zhaoping, Xiao Jing, Xue Peng, Wang Xiaoke, Yu Shali, Wu Qiyun, Zhao Xinyuan
Department of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China.
Nantong Fourth People's Hospital, Nantong, China.
Ecotoxicol Environ Saf. 2025 Jan 15;290:117736. doi: 10.1016/j.ecoenv.2025.117736.
Nanoplastics are common environmental pollutants. As of now, research has yet to explore how exposure to nanomaterials during gestation might influence the risk of developing Alzheimer's disease (AD) in offspring. Throughout the research, we assessed the AD pathology in adult offspring of mice prenatal 80 nm polystyrene nanoparticles (PS-NPs) exposure. In contrast with the control group, prenatal PS-NPs exposure obviously decreased brain tissue weight and the organ coefficient (brain weight/body weight) in adult male mice, but it only led to changes in the low-dose group of female mice. Histological examination of the adult offspring brains revealed alterations following exposure to PS-NPs during gestation. Specifically, there was a substantial reduction in neuron cells, significant changes in the number of Nissl bodies, noticeable loss of cell nucleus, and increased presence of neurofibrillary tangles in adult offspring mice exposed to PS-NPs during gestation. Furthermore, the phosphorylation levels of tau proteins at ser396 and ser199 were dramatically enhanced in the PS-NPs exposed group. Furthermore, the expression of Aβ protein was markedly increased, consistent with typical AD pathological features. Our findings suggest that being exposed to PS-NPs during pregnancy substantially raises the risk of AD in offspring.
纳米塑料是常见的环境污染物。截至目前,研究尚未探讨孕期接触纳米材料如何影响后代患阿尔茨海默病(AD)的风险。在整个研究过程中,我们评估了产前暴露于80纳米聚苯乙烯纳米颗粒(PS-NPs)的小鼠成年后代的AD病理学情况。与对照组相比,产前PS-NPs暴露明显降低了成年雄性小鼠的脑组织重量和器官系数(脑重/体重),但仅导致低剂量组雌性小鼠出现变化。对成年后代大脑的组织学检查显示,孕期暴露于PS-NPs后出现了改变。具体而言,在孕期暴露于PS-NPs的成年后代小鼠中,神经元细胞大幅减少,尼氏体数量有显著变化,细胞核明显丢失,神经原纤维缠结增多。此外,在暴露于PS-NPs的组中,tau蛋白在ser396和ser199位点的磷酸化水平显著增强。此外,Aβ蛋白的表达明显增加,这与典型的AD病理特征一致。我们的研究结果表明,孕期接触PS-NPs会大幅增加后代患AD的风险。