Hippocampal inflammation and oxidative stress following exposure to diesel exhaust nanoparticles in male and female mice

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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.

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Exposure to Air Pollution Nanoparticles: Oxidative Stress and Neuroinflammation

Ehsanifar¹,

Ss²,

Ehsanifar³

2021

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“…Our recent fi ndings support the presence of the infl ammatory eff ects in the brain tissue pathological samples whit cognitive and emotional impairment following exposure to DEPs. For example, anxiety and depression in male mice [23], hippocampal infl ammatory cytokine response, and altered morphology [19,24], and disorders in learning and memory [25,26].…”

Section: Oxidative Stress Following Air Pollution Exposure In the Strokementioning

confidence: 99%

Exposure to Ambient Ultra-Fine Particles and Stroke

Ehsanifar¹,

Ss²,

Farokhmanesh³

2021

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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.

“…Neuroinfl ammation is associated with the pathophysiology of stress-induced [21][22][23][24][25] and increases A production while decreasing its clearance, which may accelerate the occurrence and development of AD [26,27]. Signifi cant increases in A expression and tau hyperphosphorylation in the rat hippocampus have also been reported following chronic noise exposure and ApoE4 transfection, which supports the hypothesis that these factors have a cumulative eff ect on the onset and progression of AD-like neuropathological injury and shows that the synergistic interaction of these genetic and environmental factors underlies the development of ADrelated pathological changes [26,27].…”

Section: Ambient Noise and Apoe4 Causes Ad-like Neuropathologymentioning

confidence: 99%

Alzheimers Disease-Like Neuropathology Following Exposure to Ambient Noise

Ehsanifar¹,

Montazeri²,

Rafati³

2021

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Many factors play a role in the risk of dementia, including the environment. Widespread and significant worldwide exposure to noise, the severity of related health consequences, and the limited tools available to the public to protect themselves strongly support the WHO's argument that 'noise pollution is not only an environmental nuisance but also a threat to public health'. Exposures to noise from industrial activities, airport noise, or occupational noise are very important. One of the limitations of such studies is the lack of information about lifestyle habits that can play a key role in a person's risk of dementia. This review suggests that people with more exposure to ambient noise are at higher risk of Alzheimer’s Disease (AD) and dementia than other people and we examined how chronic noise exposure causes neuropathology such as AD and how it relates to ApoE4 activation. Further studies are essential to expanding global knowledge about the harmful health effects and costs of health care due to noise pollution.