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

被引:15
作者
Calderon-Garciduenas, Lilian [1 ,2 ]
Torres-Jardon, Ricardo [3 ]
Greenough, Glen P. [4 ]
Kulesza, Randy [5 ]
Gonzalez-Maciel, Angelica [6 ]
Reynoso-Robles, Rafael [6 ]
Garcia-Alonso, Griselda [2 ]
Chavez-Franco, Diana A. [2 ]
Garcia-Rojas, Edgar [2 ]
Brito-Aguilar, Rafael [2 ]
Silva-Pereyra, Hector G. [7 ]
Ayala, Alberto [8 ,9 ]
Stommel, Elijah W. [4 ]
Mukherjee, Partha S. [10 ]
机构
[1] Univ Montana, Coll Hlth, Missoula, MT 59812 USA
[2] Univ Valle Mexico, Mexico City, DF, Mexico
[3] Univ Nacl Autonoma Mexico, Inst Ciencias Atmosfera & Cambio Climat, Mexico City, DF, Mexico
[4] Geisel Sch Med Dartmouth, Dept Neurol, Hanover, NH USA
[5] Lake Erie Coll Osteopath Med, Dept Anat, Erie, PA USA
[6] Inst Nacl Pediat, Mexico City, DF, Mexico
[7] Inst Potosino Invest Cient & Tecnol AC, San Luis Potosi, San Luis Potosi, Mexico
[8] Sacramento Metropolitan Air Qual Management Dist, Sacramento, CA USA
[9] West Virginia Univ, Dept Mech & Aerosp Engn, Morgantown, WV USA
[10] Indian Stat Inst, Interdisciplinary Stat Res Unit, Kolkata, India
基金
英国科研创新办公室;
关键词
air pollution; Alzheimer's; nanoparticles; nanoneuropathology; PM2; 5; sleep disorders RBD; OSA; depression; NASAL RESPIRATORY EPITHELIUM; BEHAVIOR DISORDER; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; AIR-POLLUTION; TITANIUM-DIOXIDE; ALPHA-SYNUCLEIN; INFLAMMATORY RESPONSE; CHILDREN; DEMENTIA;
D O I
10.3389/fneur.2023.1117695
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM2.5), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting in utero, are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (A beta(1 - 42)), alpha-synuclein (alpha 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.
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页数:17
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