Mechanistic insights regarding neuropsychiatric and neuropathologic impacts of air pollution DOI
Katherine M. Rentschler, Urmila P. Kodavanti

Critical Reviews in Toxicology, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 28

Published: Dec. 10, 2024

Air pollution is a significant environmental health risk for urban areas and developing countries. may contribute to the incidence of cardiopulmonary metabolic diseases. Evidence also points role air in worsening or neurological neuropsychiatric conditions. Inhaled pollutants include compositionally differing mixtures respirable gaseous particulate components varied sizes, solubilities, chemistry. Inhalation combustibles volatile organic compounds (VOCs) other irritant matter (PM) trigger lung sensory afferents which initiate sympathetic stress response via activation hypothalamic-pituitary-adrenal (HPA) sympathetic-adrenal-medullary (SAM) axes. Activation SAM HPA axes are associated with selective inhibition hypothalamic-pituitary-gonadal (HPG) hypothalamic-pituitary-thyroid (HPT) following exposure. Regarding chronic exposure susceptible hosts, these changes become pathological by causing neuroinflammation, neurotransmitter, neuroendocrine imbalances. Soluble PM, such as metals nano-size particles translocate across olfactory, trigeminal, vagal nerves through retrograde axonal transport, systemic circulation disrupt blood-brain barrier (BBB) deposit neural tissue. Neuronal deposition metallic can have negative impact multiple molecular mechanisms. In addition translocation, release pituitary hormones, altered hormonal status resultant circulating milieu, sympathetically HPA-mediated immune markers, secondarily brain variety regulatory adrenal hormone-dependent Several reviews covering factor disorders been published, but no discuss in-depth intersection between stress-related mechanisms, thereby addressing adaptation susceptibility variations link peripheral tissue effects. The purpose this review evidence regarding neurochemical, neuroendocrine, mechanisms neuropathology from This covers bi-directional interactions raise pollution-related illness.

Language: Английский

Alzheimer and Parkinson diseases, frontotemporal lobar degeneration and amyotrophic lateral sclerosis overlapping neuropathology start in the first two decades of life in pollution exposed urbanites and brain ultrafine particulate matter and industrial nanoparticles, including Fe, Ti, Al, V, Ni, Hg, Co, Cu, Zn, Ag, Pt, Ce, La, Pr and W are key players. Metropolitan Mexico City health crisis is in progress DOI Creative Commons
Lilian Calderón‐Garcidueñas, Elijah W. Stommel, Ricardo Torres‐Jardón

et al.

Frontiers in Human Neuroscience, Journal Year: 2024, Volume and Issue: 17

Published: Jan. 12, 2024

The neuropathological hallmarks of Alzheimer’s disease (AD), Parkinson’s (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS) are present in urban children exposed to fine particulate matter (PM 2.5 ), combustion friction ultrafine PM (UFPM), industrial nanoparticles (NPs). Metropolitan Mexico City (MMC) forensic autopsies strongly suggest that anthropogenic UFPM NPs reach the brain through nasal/olfactory, lung, gastrointestinal tract, skin, placental barriers. Diesel-heavy unregulated vehicles a key source for 21.8 million MMC residents. We found hyperphosphorylated tau, beta amyloid 1-42 , α-synuclein, TAR DNA-binding protein-43 were associated with 186 (mean age 27.45 ± 11.89 years). neurovascular unit is an early anatomical target, first two decades life critical: 100% 57 aged 14.8 5.2 years had AD pathology; 25 (43.9%) AD+TDP-43; 11 (19.3%) + PD TDP-43; 2 (3.56%) +PD. Fe, Ti, Hg, Ni, Co, Cu, Zn, Cd, Al, Mg, Ag, Ce, La, Pr, W, Ca, Cl, K, Si, S, Na, C seen frontal temporal lobes, olfactory bulb, caudate, substantia nigra, locus coeruleus, medulla, cerebellum, and/or motor cortical spinal regions. Endothelial, neuronal, glial damages extensive, mitochondria, rough endoplasmic reticulum, Golgi apparatus, lysosomes. Autophagy, cell nuclear membrane damage, disruption pores heterochromatin, death present. Metals abrasion deterioration automobile catalysts electronic waste rare earth elements, i.e., lanthanum, cerium, praseodymium, entering young brains. Exposure environmental prime candidates initiating stages fatal neurodegenerative diseases. adults—surrogates polluted areas around world—exhibit AD, PD, FTLD, ALS forecasting serious health, social, economic, academic, judicial societal detrimental impact. Neurodegeneration prevention should be public health priority as problem human exposure particle pollution solvable. knowledgeable main emission sources technological options control them. What we waiting for?

Language: Английский

Citations

16
The glymphatic system and Amyotrophic lateral sclerosis DOI
Andrew Eisen, Maiken Nedergaard,

E. G. Gray

et al.

Progress in Neurobiology, Journal Year: 2024, Volume and Issue: 234, P. 102571 - 102571

Published: Jan. 22, 2024

Language: Английский

Citations

8
Microplastics suspended in dust from different indoor environments in Barranquilla, Colombia: Predominant microparticles? DOI

Angela Patricia Abad-López,

Karollayn Karina Orozco-Pérez,

Victoria A. Arana

et al.

Environmental Pollution, Journal Year: 2024, Volume and Issue: 350, P. 124023 - 124023

Published: April 23, 2024

Language: Английский

Citations

8
Air pollution, glymphatic impairment, and Alzheimer's disease DOI Creative Commons
Rashad Hussain, Uschi M. Graham, Alison Elder

et al.

Trends in Neurosciences, Journal Year: 2023, Volume and Issue: 46(11), P. 901 - 911

Published: Sept. 28, 2023

Language: Английский

Citations

22
Particulate matter-induced oxidative stress – mechanistic insights and antioxidant approaches reported in in vitro studies DOI Creative Commons
Vânia Vilas‐Boas, Nivedita Chatterjee,

Andreia Carvalho

et al.

Environmental Toxicology and Pharmacology, Journal Year: 2024, Volume and Issue: 110, P. 104529 - 104529

Published: Aug. 9, 2024

Inhaled particulate matter (PM) is a key factor in millions of yearly air pollution-related deaths worldwide. The oxidative potential PM indicates its ability to promote an environment. Excessive reactive oxygen species (ROS) can cause cell damage via stress, leading inflammation, endoplasmic reticulum airway remodeling, and various death modes (apoptosis, ferroptosis, pyroptosis). ROS also interact with macromolecules, inducing DNA epigenetic modifications, disrupting homeostasis. These effects have been studied extensively vitro confirmed vivo. This review explores the airborne particles PM-induced ROS-mediated cellular observed vitro, highlighting link between described latest literature. analyzes on damage, repair, carcinogenicity, epigenetics. Additionally, developments antioxidants prevent ROS's harmful are described, providing future perspectives topic.

Language: Английский

Citations

5
Single-domain magnetic particles with motion behavior under electromagnetic AC and DC fields are a fatal cargo in Metropolitan Mexico City pediatric and young adult early Alzheimer, Parkinson, frontotemporal lobar degeneration and amyotrophic lateral sclerosis and in ALS patients DOI Creative Commons
Ana Laura Calderón‐Garcidueñas, Rubén Cejudo, Elijah W. Stommel

et al.

Frontiers in Human Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Aug. 23, 2024

Metropolitan Mexico City (MMC) children and young adults exhibit overlapping Alzheimer Parkinsons’ diseases (AD, PD) TAR DNA-binding protein 43 pathology with magnetic ultrafine particulate matter (UFPM) industrial nanoparticles (NPs). We studied magnetophoresis, electron microscopy energy-dispersive X-ray spectrometry in 203 brain samples from 14 children, 27 adults, ALS cases/controls. Saturation isothermal remanent magnetization (SIRM), capturing magnetically unstable FeNPs ̴ 20nm, was higher caudate, thalamus, hippocampus, putamen, motor regions subcortical vs. cortical SIRM MMC ≤ 40y. Motion behavior associated exposures 25–100 mT exhibited IRM saturated curves at 50–300 to change NPs position and/or orientation situ . Targeted profiles moving under AC/AD fields could distinguish controls. Motor neuron accumulation potentially interferes action potentials, ion channels, nuclear pores enhances the membrane insertion process when coated lipopolysaccharides. TEM EDX showed 7–20 nm NP Fe, Ti, Co, Ni, V, Hg, W, Al, Zn, Ag, Si, S, Br, Ce, La, Pr abnormal neural vascular organelles. Brain of particles start childhood cytotoxic, hyperthermia, free radical formation, motion 30–50 μT (DC fields) are critical given ubiquitous electric induce damage. Magnetic UFPM/NPs a fatal cargo children’s brains, preventable AD, PD, FTLD, environmental threat. Billions people risk. clearly poisoning ourselves.

Language: Английский

Citations

5
Environmental Risk Factors for Parkinson's Disease: A Critical Review and Policy Implications DOI Creative Commons
Kajsa Brolin, Eva Schaeffer, Ashvin Kuri

et al.

Movement Disorders, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 27, 2024

Abstract The age‐standardized prevalence of Parkinson's disease (PD) has increased substantially over the years and is expected to increase further. This emphasizes need identify modifiable risk factors PD, which could form a logical entry point for prevention PD. World Health Organization (WHO) recommended reducing exposure specific environmental that have been reported be associated with in particular pesticides, trichloroethylene (TCE), air pollution. In this review we critically evaluate epidemiological biological evidence on associations these PD whether putative are causal. We conclude when considered isolation, it difficult determine causal, large part because decades‐long lag between relevant exposures incidence manifest However, tandem from complementary research lines (such as animal models), increasingly likely reflect harmful causal effects. Fundamentally, whilst highlight some gaps require further attention, believe current base sufficiently strong enough support our call stronger policy action. © 2024 Author(s). Movement Disorders published by Wiley Periodicals LLC behalf International Parkinson Disorder Society.

Language: Английский

Citations

4
Sleep and Arousal Hubs and Ferromagnetic Ultrafine Particulate Matter and Nanoparticle Motion Under Electromagnetic Fields: Neurodegeneration, Sleep Disorders, Orexinergic Neurons, and Air Pollution in Young Urbanites DOI Creative Commons
Lilian Calderón‐Garcidueñas, Rubén Cejudo, Elijah W. Stommel

et al.

Toxics, Journal Year: 2025, Volume and Issue: 13(4), P. 284 - 284

Published: April 8, 2025

Air pollution plays a key role in sleep disorders and neurodegeneration. Alzheimer’s disease (AD), Parkinson’s (PD), and/or transactive response DNA-binding protein TDP-43 neuropathology have been documented children young adult forensic autopsies the metropolitan area of Mexico City (MMC), along with disorders, cognitive deficits, MRI brain atrophy seemingly healthy populations. Ultrafine particulate matter (UFPM) industrial nanoparticles (NPs) reach urbanites’ brains through nasal/olfactory, lung, gastrointestinal tract, placental barriers. We Fe UFPM/NPs neurovascular units, as well lateral hypothalamic nucleus orexinergic neurons, thalamus, medullary, pontine, mesencephalic reticular formation, pinealocytes. quantified ferromagnetic materials arousal hubs examined their motion behavior to low magnetic fields MMC autopsy samples from nine 25 adults AD, PD, neuropathology. Saturated isothermal remanent magnetization curves at 50–300 mT were associated UFPM/NP accumulation sleep/awake 30–50 µT (DC fields) exposure. Brain exposed anthropogenic PM found be sensitive fields, behaviors that potentially linked early development progression fatal neurodegenerative diseases disorders. Single-domain orexin system, arousal, sleep, autonomic regions, are neurodegeneration, behavioral impairment, need identify higher risk monitor environmental UFPM NP emissions exposures fields. Ubiquitous ferrimagnetic particles field threat global health.

Language: Английский

Citations

0
Associations of air pollution with all-cause dementia, Alzheimer’s disease, and vascular dementia: a prospective cohort study based on 437,932 participants from the UK biobank DOI Creative Commons
Shiqi Yuan, Xiaxuan Huang, Luming Zhang

et al.

Frontiers in Neuroscience, Journal Year: 2023, Volume and Issue: 17

Published: Aug. 4, 2023

To prospectively assess whether air pollution, including PM2.5, PM10, and NOx, is associated with the risk of all-cause dementia, Alzheimer's disease (AD), vascular to investigate potential relationship between pollution genetic susceptibility in development AD.Our study included 437,932 participants from UK Biobank a median follow-up period over 10 years. Using Cox proportional hazards model, we found that exposed PM2.5 levels ≥10 μg/m3 had higher developing dementia (HR = 1.1; 95% CI: 1.05-1.28; p < 0.05) compared group <10 μg/m3. However, there was no significant association PM10 ≥15 AD, or when <15 On other hand, NOx ≥50 significantly 1.14; 1.02-1.26; AD 1.26; 1.08-1.48; <50 Furthermore, examined combined effect (PM2.5, NOx) score (AD-GRS) on using model. Among high AD-GRS, those 1.36; 1.03-1.18; 0.05). Regardless pollutant NOx), AD-GRS increased AD. Similar results were obtained assessing multiple variables inverse probability treatment weighting (IPTW).Our findings indicate individuals living areas are at dementia. Moreover, demonstrated an particularly presence ≥ 50

Language: Английский

Citations

9
History of ALS and the competing theories on pathogenesis: IFCN handbook chapter DOI Creative Commons
Andrew Eisen, Steve Vucic, Hiroshi Mitsumoto

et al.

Clinical Neurophysiology Practice, Journal Year: 2023, Volume and Issue: 9, P. 1 - 12

Published: Dec. 12, 2023

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disorder of the human motor system, first described in 19th Century. The etiology ALS appears to be multifactorial, with complex interaction genetic, epigenetic, and environmental factors underlying onset disease. Importantly, there are no known naturally occurring animal models, transgenic mouse models fail faithfully reproduce as it manifests patients. Debate site remain, three competing theories proposed, including (i)

Language: Английский

Citations

7