Exposure to ambient dusty particulate matter impairs spatial memory and hippocampal LTP by increasing brain inflammation and oxidative stress in rats

Hajipour, Somayeh; Farbood, Yaghoob; Gharib-Naseri, Mohammad Kazem; Goudarzi, Gholamreza; Rashno, Mohammad; Maleki, Heidar; Bakhtiari, Nima; Nesari, Ali; Khoshnam, Seyed Esmaeil; Dianat, Mahin; Sarkaki, Behjat; Sarkaki, Alireza

doi:10.1016/j.lfs.2019.117210

Cited by 55 publications

(21 citation statements)

References 62 publications

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“…These results suggest that subchronic exposure to environmental levels of PM 2.5 did not induce prominent cognitive or motor dysfunction. Previous studies revealed negative performances in MWM [ 43 , 44 ], Barnes maze task, force swimming [ 45 ], and novel object recognition (NOR) test [ 46 ] in rodent models after subchronic or chronic exposure to higher concentrations of PM. However, no obvious behavioral differences in the MWM [ 32 , 47 ], Y maze, force swimming [ 38 ], or rotarod test [ 28 ] were found in rodents under relatively lower concentration exposure to PM.…”

Section: Discussionmentioning

confidence: 99%

Three month inhalation exposure to low-level PM2.5 induced brain toxicity in an Alzheimer’s disease mouse model

et al. 2021

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Although numerous epidemiological studies revealed an association between ambient fine particulate matter (PM2.5) exposure and Alzheimer’s disease (AD), the PM2.5-induced neuron toxicity and associated mechanisms were not fully elucidated. The present study assessed brain toxicity in 6-month-old female triple-transgenic AD (3xTg-AD) mice following subchronic exposure to PM2.5 via an inhalation system. The treated mice were whole-bodily and continuously exposed to real-world PM2.5 for 3 months, while the control mice inhaled filtered air. Changes in cognitive and motor functions were evaluated using the Morris Water Maze and rotarod tests. Magnetic resonance imaging analysis was used to record gross brain volume alterations, and tissue staining with hematoxylin and eosin, Nissl, and immunohistochemistry methods were used to monitor pathological changes in microstructures after PM2.5 exposure. The levels of AD-related hallmarks and the oxidative stress biomarker malondialdehyde (MDA) were assessed using Western blot analysis and liquid chromatography-mass spectrometry, respectively. Our results showed that subchronic exposure to environmental levels of PM2.5 induced obvious neuronal loss in the cortex of exposed mice, but without significant impairment of cognitive and motor function. Increased levels of phosphorylated-tau and MDA were also observed in olfactory bulb or hippocampus after PM2.5 exposure, but no amyloid pathology was detected, as reported in previous studies. These results revealed that a relatively lower level of PM2.5 subchronic exposure from the environmental atmosphere still induced certain neurodegenerative changes in the brains of AD mice, especially in the olfactory bulb, entorhinal cortex and hippocampus, which is consistent with the nasal entry and spreading route for PM exposure. Systemic factors may also contribute to the neuronal toxicity. The effects of PM2.5 after a more prolonged exposure period are needed to establish a more comprehensive picture of the PM2.5-mediated development of AD.

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Section: Discussionmentioning

confidence: 99%

Three month inhalation exposure to low-level PM2.5 induced brain toxicity in an Alzheimer’s disease mouse model

et al. 2021

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“…First, they can induce the release of proinflammatory mediators leading to chronic respiratory and systemic inflammation [ 27 ], thereby affecting the BBB and ultimately triggering neural-immune interaction and resulting in increased production of ROS and chronic oxidative stress contributing to an Alzheimer phenotype in exposed children [ 28 ]. Second, the particles can damage the BBB through the direct formation of ROS and thereby alter the permeability of the barrier [ 29 , 30 ]. Third, there can be mechanical stimulation of specific mechano-receptors in pulmonary tissue leading to the lung arc reflex [ 31 , 32 ] and sympathetic activation with the release of vasoconstrictors such as catecholamines [ 33 ].…”

Section: Pathophysiology Of Air-pollution-induced Disordersmentioning

confidence: 99%

“…Activation of NLRP3 in microglia exacerbates diesel exhaust particles-induced impairment in learning and memory in mice [133] Impairment of learning and memory, induction of oxidative stress and dysregulation of monoamine neurotransmitters in the brains of mice by exposure to volatile organic compounds and carbon monoxide mixtures [134] PM2.5, SO 2 and NO 2 co-exposure impairs neurobehavior and induces mitochondrial injuries in the mouse brain [135] Effects of diesel engine exhaust origin secondary organic aerosols on novel object recognition ability and maternal behavior in mice [136] Exposure to ambient dusty particulate matter impairs spatial memory and hippocampal long-term potentiation by increasing brain inflammation and oxidative stress in rats [30] Mental disorders…”

Section: Studies and Major Outcomesmentioning

confidence: 99%

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Hahad

Lelieveld

Birklein

et al. 2020

IJMS

281

107

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Exposure to ambient air pollution is a well-established determinant of health and disease. The Lancet Commission on pollution and health concludes that air pollution is the leading environmental cause of global disease and premature death. Indeed, there is a growing body of evidence that links air pollution not only to adverse cardiorespiratory effects but also to increased risk of cerebrovascular and neuropsychiatric disorders. Despite being a relatively new area of investigation, overall, there is mounting recent evidence showing that exposure to multiple air pollutants, in particular to fine particles, may affect the central nervous system (CNS) and brain health, thereby contributing to increased risk of stroke, dementia, Parkinson’s disease, cognitive dysfunction, neurodevelopmental disorders, depression and other related conditions. The underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests inflammation and oxidative stress to be crucial factors in the pathogenesis of air pollution-induced disorders, driven by the enhanced production of proinflammatory mediators and reactive oxygen species in response to exposure to various air pollutants. From a public health perspective, mitigation measures are urgent to reduce the burden of disease and premature mortality from ambient air pollution.

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“…While this has not been demonstrated in studies of WFS-derived PM, there are reports of altered BBB permeability following AAP exposure. 58,59 Additionally, AWS has been demonstrated to activate the nuclear factor kappa B (NF-kB) pathway as well as increase the release of tumor necrosis factor alpha (TNF-α) in mouse peritoneal macrophages. 56 This cascade leads to the systemic release of proinflammatory cytokines (IL-1β, 6, 12, 18) and is known to regulate BBB structural integrity.…”

Section: Woodsmoke Exposurementioning

confidence: 99%

Influence of Woodsmoke Exposure on Molecular Mechanisms Underlying Alzheimer’s Disease: Existing Literature and Gaps in Our Understanding

Schuller

Montrose

2020

Genet Epigenet

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Woodsmoke poses a significant health risk as a growing component of ambient air pollution in the United States. While there is a long history of association between woodsmoke exposure and diseases of the respiratory, circulatory, and cardiovascular systems, recent evidence has linked woodsmoke exposure to cognitive dysfunction, including Alzheimer’s disease dementia. Alzheimer’s disease is a progressive neurodegenerative disorder with largely idiopathic origins and no known cure. Here, we explore the growing body of literature which relates woodsmoke-generated and ambient air pollution particulate matter exposure to Alzheimer’s disease (AD) onset or exacerbation, in the context of an inflammation-centric view of AD. Epigenetic modifications, specifically changes in DNA methylation patterns, are well documented following woodsmoke exposure and have been shown to influence disease-favoring inflammatory cascades, induce oxidative stress, and modulate the immune response in vitro, in vivo, and in humans following exposure to air pollution. Though the current status of the literature does not allow us to draw definitive conclusions linking these events, this review highlights the need for additional work to fill gaps in our understanding of the directionality, causality, and susceptibility throughout the life course.

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Exposure to ambient dusty particulate matter impairs spatial memory and hippocampal LTP by increasing brain inflammation and oxidative stress in rats

Cited by 55 publications

References 62 publications

Three month inhalation exposure to low-level PM2.5 induced brain toxicity in an Alzheimer’s disease mouse model

Three month inhalation exposure to low-level PM2.5 induced brain toxicity in an Alzheimer’s disease mouse model

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress

Influence of Woodsmoke Exposure on Molecular Mechanisms Underlying Alzheimer’s Disease: Existing Literature and Gaps in Our Understanding

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