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Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option
Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM(2.5)), 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 hyperphosp...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10010440/ https://www.ncbi.nlm.nih.gov/pubmed/36923490 http://dx.doi.org/10.3389/fneur.2023.1117695 |
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author | 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. |
author_facet | 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. |
author_sort | Calderón-Garcidueñas, Lilian |
collection | PubMed |
description | Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM(2.5)), 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 (Aβ(1 − 42)), 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. |
format | Online Article Text |
id | pubmed-10010440 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-100104402023-03-14 Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option 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. Front Neurol Neurology Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM(2.5)), 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 (Aβ(1 − 42)), 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. Frontiers Media S.A. 2023-02-27 /pmc/articles/PMC10010440/ /pubmed/36923490 http://dx.doi.org/10.3389/fneur.2023.1117695 Text en Copyright © 2023 Calderón-Garcidueñas, Torres-Jardón, Greenough, Kulesza, González-Maciel, Reynoso-Robles, García-Alonso, Chávez-Franco, García-Rojas, Brito-Aguilar, Silva-Pereyra, Ayala, Stommel and Mukherjee. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neurology 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. Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title | Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title_full | Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title_fullStr | Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title_full_unstemmed | Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title_short | Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—Denial is not an option |
title_sort | sleep matters: neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders—denial is not an option |
topic | Neurology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10010440/ https://www.ncbi.nlm.nih.gov/pubmed/36923490 http://dx.doi.org/10.3389/fneur.2023.1117695 |
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