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睡眠至关重要:神经退行性变谱的异质性、燃烧与摩擦产生的超细颗粒、工业纳米颗粒污染以及睡眠障碍——否认并非可行之策。

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders-Denial is not an option.

作者信息

Calderón-Garcidueñas Lilian, Torres-Jardón Ricardo, Greenough Glen P, Kulesza Randy, González-Maciel Angélica, Reynoso-Robles Rafael, García-Alonso Griselda, Chávez-Franco Diana A, García-Rojas Edgar, Brito-Aguilar Rafael, Silva-Pereyra Héctor G, Ayala Alberto, Stommel Elijah W, Mukherjee Partha S

机构信息

College of Health, The University of Montana, Missoula, MT, United States.

Universidad del Valle de México, Mexico City, Mexico.

出版信息

Front Neurol. 2023 Feb 27;14:1117695. doi: 10.3389/fneur.2023.1117695. eCollection 2023.

Abstract

Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting , are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (Aβ), α-synuclein (α syn) and TAR DNA-binding protein 43 (TDP-43), hallmarks of Alzheimer's (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). UFPM from anthropogenic and natural sources and NPs enter the brain through the nasal/olfactory pathway, lung, gastrointestinal (GI) tract, skin, and placental barriers. On a global scale, the most important sources of outdoor UFPM are motor traffic emissions. This study focuses on the neuropathology heterogeneity and overlap of AD, PD, FTLD, and ALS in older adults, their similarities with the neuropathology of young, highly exposed urbanites, and their strong link with sleep disorders. Critical information includes how this UFPM and NPs cross all biological barriers, interact with brain soluble proteins and key organelles, and result in the oxidative, endoplasmic reticulum, and mitochondrial stress, neuroinflammation, DNA damage, protein aggregation and misfolding, and faulty complex protein quality control. The brain toxicity of UFPM and NPs makes them powerful candidates for early development and progression of fatal common neurodegenerative diseases, all having sleep disturbances. A detailed residential history, proximity to high-traffic roads, occupational histories, exposures to high-emission sources (i.e., factories, burning pits, forest fires, and airports), indoor PM sources (tobacco, wood burning in winter, cooking fumes, and microplastics in house dust), and consumption of industrial NPs, along with neurocognitive and neuropsychiatric histories, are critical. Environmental pollution is a ubiquitous, early, and cumulative risk factor for neurodegeneration and sleep disorders. Prevention of deadly neurological diseases associated with air pollution should be a public health priority.

摘要

持续暴露于无处不在的室外/室内细颗粒物(PM),包括燃烧和摩擦产生的超细颗粒物(UFPM)以及工业纳米颗粒(NP),从一开始就与儿童早期和青年期异常的神经蛋白积累有关,包括过度磷酸化的tau蛋白(p-tau)、β-淀粉样蛋白(Aβ)、α-突触核蛋白(α syn)和TAR DNA结合蛋白43(TDP-43),这些都是阿尔茨海默病(AD)、帕金森病(PD)、额颞叶痴呆(FTLD)和肌萎缩侧索硬化症(ALS)的特征。来自人为和自然源的UFPM以及NP通过鼻/嗅觉途径、肺、胃肠道(GI)、皮肤和胎盘屏障进入大脑。在全球范围内,室外UFPM的最重要来源是机动车尾气排放。本研究聚焦于老年人中AD、PD、FTLD和ALS的神经病理学异质性和重叠、它们与高暴露年轻城市居民神经病理学的相似性以及它们与睡眠障碍的紧密联系。关键信息包括这些UFPM和NP如何穿过所有生物屏障、与脑可溶性蛋白和关键细胞器相互作用,以及导致氧化应激、内质网应激和线粒体应激、神经炎症、DNA损伤、蛋白质聚集和错误折叠以及复杂蛋白质质量控制故障。UFPM和NP的脑毒性使它们成为致命常见神经退行性疾病早期发展和进展的有力候选因素,所有这些疾病都伴有睡眠障碍。详细的居住史、与交通繁忙道路的距离、职业史、对高排放源(如工厂、焚烧坑、森林火灾和机场)的暴露、室内PM源(烟草、冬季木材燃烧、烹饪油烟和室内灰尘中的微塑料)以及工业NP的接触,连同神经认知和神经精神病史,都至关重要。环境污染是神经退行性变和睡眠障碍普遍存在、早期且累积的风险因素。预防与空气污染相关的致命神经系统疾病应成为公共卫生的优先事项。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/10010440/188570d6ad93/fneur-14-1117695-g0001.jpg

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