scholarly journals Exposure to Ambient Ultra-Fine Particles and Stroke

2021 ◽  
Vol 2 (10) ◽  
pp. 954-958
Author(s):  
Mojtaba Ehsanifar ◽  
Banihashemian SS ◽  
Farzaneh Farokhmanesh
Keyword(s):  
Air Pollution ◽  
Fine Particles ◽  
Olfactory Nerve ◽  
Preliminary Review ◽  
Key Factors ◽  
Pm 2.5 ◽  
Significant Research ◽  
Ultra Fine Particles ◽  
The Brain ◽  
And Oxidative Stress

Stroke is one of the main causes of death attributed to air pollution. Significant research has now shown that urban air pollutants exposure has been established as a source of neuroinflammation and oxidative stress that causes Central Nervous System (CNS) disease. Transition metals, Particulate Matter (PM) including fine particles (PM ≤ 2.5 μm, PM 2.5) and ultra-fine particles (UFPs, PM <0.1 μm, PM 0.1), nitrogen oxide, and ozone are potent or oxidant that capable of producing Reactive Oxygen Species (ROS) can reach the brain and affect CNS health. Numerous biological mechanisms are responsible that are not well understood. Recent studies suggest that changes in the Blood-Brain Barrier (BBB) and or leakage and transmission along the olfactory nerve into the Olfactory Bulb (OB) and microglial activation are the key factors of CNS damage following exposure to air pollution. This preliminary review cites evidence that ambient PM exposure is one of the causes of stroke.

Air pollution and your brain: what do you need to know right now

2014 ◽  
Vol 16 (04) ◽  
pp. 329-345 ◽  
Author(s):  
Lilian Calderón-Garcidueñas ◽  
Ana Calderón-Garcidueñas ◽  
Ricardo Torres-Jardón ◽  
José Avila-Ramírez ◽  
Randy J. Kulesza ◽  
...  
Keyword(s):  
Public Health ◽  
Air Pollution ◽  
Particulate Matter ◽  
Fine Particles ◽  
Public Health Problem ◽  
The United States ◽  
Global Public Health ◽  
Health Providers ◽  
Parkinson’S Diseases ◽  
The Brain

Research links air pollution mostly to respiratory and cardiovascular disease. The effects of air pollution on the central nervous system (CNS) are not broadly recognized. Urban outdoor pollution is a global public health problem particularly severe in megacities and in underdeveloped countries, but large and small cities in the United States and the United Kingom are not spared. Fine and ultrafine particulate matter (UFPM) defined by aerodynamic diameter (&lt;2.5-μm fine particles, PM2.5, and &lt;100-nm UFPM) pose a special interest for the brain effects given the capability of very small particles to reach the brain. In adults, ambient pollution is associated to stroke and depression, whereas the emerging picture in children show significant systemic inflammation, immunodysregulation at systemic, intratechal and brain levels, neuroinflammation and brain oxidative stress, along with the main hallmarks of Alzheimer and Parkinson’s diseases: hyperphosphorilated tau, amyloid plaques and misfoldedα-synuclein. Animal models exposed to particulate matter components show markers of both neuroinflammation and neurodegeneration. Epidemiological, cognitive, behavioral and mechanistic studies into the association between air pollution exposures and the development of CNS damage particularly in children are of pressing importance for public health and quality of life. Primary health providers have to include a complete prenatal and postnatal environmental and occupational history to indoor and outdoor toxic hazards and measures should be taken to prevent or reduce further exposures.

scholarly journals Exposure to Air Pollution Nanoparticles: Oxidative Stress and Neuroinflammation

2021 ◽  
Vol 2 (10) ◽  
pp. 964-976
Author(s):  
Mojtaba Ehsanifar ◽  
Banihashemian SS ◽  
Masoud Ehsanifar
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Air Pollutants ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Urban Air ◽  
Pm 2.5 ◽  
The Central Nervous System ◽  
New Evidence ◽  
The Brain

Urban air pollutants exposure is known as a source of neuroinflammation and oxidative stress that causes the Central Nervous System (CNS) and neuropathology disease. Transition metals, Particulate Matter (PM), including PM 2.5 (PM <2.5 μm) and PM 0.1 (PM <0.1μm), nitrogen oxides and ozone are of potent or oxidant capable of producing Reactive Oxygen Species (ROS). Redox-sensitive pathways can be caused by oxidative stress, leading to various biological processes, including inflammation and cell death. The incidence of Alzheimer's Disease (AD) and Parkinson's Disease (PD) and stroke are associated with exposure to air pollution. Some recent findings suggest that urban air pollutants reach the brain in addition to pulmonary and cardiovascular diseases and affect the CNS health too. While the underlying CNS pathology mechanisms induced air pollutants exposure are not well understood, recent studies show that changes in Blood Brain Barrier (BBB) and microglial activation are key components. In this work, we reviewed the new evidence of the mechanisms by which ambient air pollution reach the brain and activate innate immune response as a source of oxidative stress and neuroinflammatory factors.

Health & Hope Oasis Air Pollution the Silent Killer

2020 ◽  
pp. 1-3
Author(s):  
Muhammad Shoaib Hashmi ◽  
Keyword(s):  
Air Pollution ◽  
Urban Areas ◽  
Respiratory Diseases ◽  
Fine Particles ◽  
Early Death ◽  
Motor Vehicles ◽  
Outdoor Air ◽  
Pm 2.5 ◽  
Outdoor Air Pollution ◽  
Harmful Emissions

Outdoor air pollution is a leading cause of early death, chronic disease, and disability. Motor vehicles are a major contributor to outdoor air pollution, exposing vulnerable population to especially high levels of harmful emissions in urban areas and near major roadways. Fine particles or particulate matter with a diameter of 2.5 micrometers or less (PM 2.5), are among the most harmful vehicle pollutants and are associated with a range of health impacts including cardiovascular and respiratory diseases, lung cancer, and infant mortality.

scholarly journals Aging Brain: Prevention of Oxidative Stress by Vitamin E and Exercise

2009 ◽  
Vol 9 ◽  
pp. 366-372 ◽  
Author(s):  
Sambe Asha Devi
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Cognitive Decline ◽  
Middle Age ◽  
Neuronal Loss ◽  
Aging Brain ◽  
Key Factors ◽  
Esterase Inhibitors ◽  
The Brain ◽  
And Oxidative Stress

With aging, the brain undergoes neuronal loss in many areas. Although the loss of cells in the cerebral cortex, in particular the frontal cortex, has been recognized with aging, the influence of synaptic losses has a larger impact on cognitive decline. Much of the recent research on animals, as well as humans, has been aimed at slowing the cognitive decline through enrichment, and it has been found that the key factors are antioxidants and exercise. Several reports support the concept that regular supplementation of vitamin E and physical activity from as early as middle age can slow the cognitive decline observed during the later years. A few studies have also suggested that exercise is analogous to acetylcholine esterase inhibitors that are also used extensively to treat cognitive impairment and dementia in Alzheimer's disease. In addition, reports also support that vitamin E and exercise may act synergistically to overcome free radical injury and oxidative stress in the aging brain.

Studies of copper selenide ultrafine particles by newly developed gas evaporation method

1990 ◽  
Vol 48 (4) ◽  
pp. 306-307
Author(s):  
Chihiro Kaito ◽  
Yoshio Saito
Keyword(s):  
Crystal Structure ◽  
Ultrafine Particles ◽  
Fine Particles ◽  
Production Method ◽  
Atmospheric Temperature ◽  
Copper Selenide ◽  
Quartz Boat ◽  
Selenium Vapor ◽  
Ar Gas ◽  
Ultra Fine Particles

The direct evaporation of metallic oxides or sulfides does not always given the same compounds with starting material, i.e. decomposition took place. Since the controll of the sulfur or selenium vapors was difficult, a similar production method for oxide particles could not be used for preparation of such compounds in spite of increasing interest in the fields of material science, astrophysics and mineralogy. In the present paper, copper metal was evaporated from a molybdenum silicide heater which was proposed by us to produce the ultra-fine particles in reactive gas as shown schematically in Figure 1. Typical smoke by this method in Ar gas at a pressure of 13 kPa is shown in Figure 2. Since the temperature at a location of a few mm below the heater, maintained at 1400° C , were a few hundred degrees centigrade, the selenium powder in a quartz boat was evaporated at atmospheric temperature just below the heater. The copper vapor that evaporated from the heater was mixed with the stream of selenium vapor,and selenide was formed near the boat. If then condensed by rapid cooling due to the collision with inert gas, thus forming smoke similar to that from the metallic sulfide formation. Particles were collected and studied by a Hitachi H-800 electron microscope.Figure 3 shows typical EM images of the produced copper selenide particles. The morphology was different by the crystal structure, i.e. round shaped plate (CuSe;hexagona1 a=0.39,C=l.723 nm) ,definite shaped p1 ate(Cu5Se4;Orthorhombic;a=0.8227 , b=1.1982 , c=0.641 nm) and a tetrahedron(Cu1.8Se; cubic a=0.5739 nm). In the case of compound ultrafine particles there have been no observation for the particles of the tetrahedron shape. Since the crystal structure of Cu1.8Se is the anti-f1uorite structure, there has no polarity.

Electromagnetic field in Alzheimer’s disease: a literature review of recent preclinical and clinical studies

2020 ◽  
Vol 17 ◽  
Author(s):  
Reem Habib Mohamad Ali Ahmad ◽  
Marc Fakhoury ◽  
Nada Lawand
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
In Vivo Studies ◽  
Key Factors ◽  
Potential Benefits ◽  
Preclinical And Clinical Studies ◽  
The Brain

: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the progressive loss of neurons leading to cognitive and memory decay. The main signs of AD include the irregular extracellular accumulation of amyloidbeta (Aβ) protein in the brain and the hyper-phosphorylation of tau protein inside neurons. Changes in Aβ expression or aggregation are considered key factors in the pathophysiology of sporadic and early-onset AD and correlate with the cognitive decline seen in patients with AD. Despite decades of research, current approaches in the treatment of AD are only symptomatic in nature and are not effective in slowing or reversing the course of the disease. Encouragingly, recent evidence revealed that exposure to electromagnetic fields (EMF) can delay the development of AD and improve memory. This review paper discusses findings from in vitro and in vivo studies that investigate the link between EMF and AD at the cellular and behavioural level, and highlights the potential benefits of EMF as an innovative approach for the treatment of AD.

scholarly journals Gut Microbiota and Dysbiosis in Alzheimer’s Disease: Implications for Pathogenesis and Treatment

2020 ◽  
Vol 57 (12) ◽  
pp. 5026-5043 ◽  
Author(s):  
Shan Liu ◽  
Jiguo Gao ◽  
Mingqin Zhu ◽  
Kangding Liu ◽  
Hong-Liang Zhang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gut Microbiota ◽  
Gut Dysbiosis ◽  
Bidirectional Communication ◽  
Significant Research ◽  
Novel Therapeutic Strategies ◽  
The Brain ◽  
Brain Homeostasis ◽  
Gut Microbiota Composition

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.

scholarly journals UV-induced neuronal degeneration in the rat cerebral cortex

2021 ◽  
Author(s):  
Mariko Nakata ◽  
Masayuki Shimoda ◽  
Shinya Yamamoto
Keyword(s):  
Uv Irradiation ◽  
Neuronal Degeneration ◽  
Uv Light ◽  
Brain Lesion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Heme Oxygenase 1 ◽  
Dependent Manner ◽  
Focal Brain Injury ◽  
The Brain ◽  
And Oxidative Stress

Abstract Irradiation with ultraviolet (UV) light on the cortical surface can induce a focal brain lesion (UV lesion) in rodents. In the present study, we investigated the process of establishing a UV lesion. Rats underwent UV irradiation (365 nm wavelength, 2.0 mWh) over the dura, and time-dependent changes in the cortical tissue were analyzed histologically. We found that the majority of neurons in the lesion started to degenerate within 24 hours and the rest disappeared within 5 days after irradiation. UV-induced neuronal degeneration progressed in a layer-dependent manner. Moreover, UV-induced terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positivity and heme oxygenase-1 (HO-1) immunoreactivity were also detected. These findings suggest that UV irradiation in the brain can induce gradual neural degeneration and oxidative stress. Importantly, UV vulnerability may vary among cortical layers. UV-induced cell death may be due to apoptosis; however, there remains a possibility that UV-irradiated cells were degenerated via processes other than apoptosis. The UV lesion technique will not only assist in investigating brain function at a targeted site but may also serve as a pathophysiological model of focal brain injury and/or neurodegenerative disorders.

scholarly journals SHR/NCrl rats as a model of ADHD can be discriminated from controls based on their brain, blood, or urine metabolomes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Camille Dupuy ◽  
Pierre Castelnau ◽  
Sylvie Mavel ◽  
Antoine Lefevre ◽  
Lydie Nadal-Desbarats ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Attention Deficit Hyperactivity Disorder ◽  
Animal Model ◽  
Metabolic Pathways ◽  
Neurodevelopmental Disorder ◽  
Hyperactivity Disorder ◽  
Pathophysiological Condition ◽  
The Brain ◽  
And Oxidative Stress ◽  
Peripheral Samples

AbstractAttention-Deficit Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorder characterized by inattention, impulsivity, and hyperactivity. The neurobiological mechanisms underlying ADHD are still poorly understood, and its diagnosis remains difficult due to its heterogeneity. Metabolomics is a recent strategy for the holistic exploration of metabolism and is well suited for investigating the pathophysiology of diseases and finding molecular biomarkers. A few clinical metabolomic studies have been performed on peripheral samples from ADHD patients but are limited by their access to the brain. Here, we investigated the brain, blood, and urine metabolomes of SHR/NCrl vs WKY/NHsd rats to better understand the neurobiology and to find potential peripheral biomarkers underlying the ADHD-like phenotype of this animal model. We showed that SHR/NCrl rats can be differentiated from controls based on their brain, blood, and urine metabolomes. In the brain, SHR/NCrl rats displayed modifications in metabolic pathways related to energy metabolism and oxidative stress further supporting their importance in the pathophysiology of ADHD bringing news arguments in favor of the Neuroenergetic theory of ADHD. Besides, the peripheral metabolome of SHR/NCrl rats also shared more than half of these differences further supporting the importance of looking at multiple matrices to characterize a pathophysiological condition of an individual. This also stresses out the importance of investigating the peripheral energy and oxidative stress metabolic pathways in the search of biomarkers of ADHD.

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