Traffic-Related Air Pollution and Neurodegenerative Diseases: Epidemiological and Experimental Evidence, and Potential Underlying Mechanisms

Costa, Lucio G.

doi:10.1016/bs.ant.2017.07.001

Cited by 9 publications

(24 citation statements)

References 249 publications

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“…Since then there has been almost a 20year gap in research on air pollution and stroke and dementia, but over the last two decades, the interest in such research has considerably increased. 1,19 The nature of air pollution Air pollution is a global and diffuse contamination by chemical compounds and sometimes biological materials.…”

Section: History Of Air Pollutionmentioning

confidence: 99%

“…3,11,12 Effect of air pollution on dementia and cognitive decline occurrence (Table 2) The number of well-conducted cohort studies reporting an association between air pollution exposure and dementia is increasing. Recent reviews by Xu et al 36 and Costa 19 devoted to air pollution and dementia provided strong evidence of the association of cognitive decline with PM2.5, PM 10, O 3 , and NO 2 exposure. [37][38][39][40][41][42][43][44][45] There is also evidence of the association of Alzheimer's disease (AD) occurrence with O 3 , PM2.5, PM10, NO 2 and NOX exposure, [46][47][48][49][50] and the association of vascular dementia (VD) with O 3 , NO 2 , and NOX exposure.…”

Section: Global Burden Of Diseasementioning

confidence: 99%

“…Furthermore, leucocyte telomere length, considered a biomarker of biological aging 55,56 associated with myocardial infarction, stroke, type 2 diabetes mellitus, 57 is reduced in dementia induced by air pollution. 19,36,58 Magnetic-resonance analyses of human brains exposed to air pollution showed the presence of nanoparticles of magnetite, a biological product of iron oxide which has a ferromagnetic signal that may be generated by the PM exposure. 23 This could explain the direct relationship observed between PM air pollution and AD.…”

Section: Global Burden Of Diseasementioning

confidence: 99%

“…23,51,54 A causal relationship between two other important biomarkers of AD (reelin and glutamate) exposure to air pollution has also been suggested. 19 Reelin is an extracellular glycoprotein which plays a major role in neuronal migration and neuronal polarity. In adulthood, reelin is expressed in GABAergic interneurons of hippocampus modulating learning and memory functions.…”

Section: Global Burden Of Diseasementioning

confidence: 99%

“…In adulthood, reelin is expressed in GABAergic interneurons of hippocampus modulating learning and memory functions. 19 Glutamatergic synapses are essential for learning and memory processing and there is evidence suggesting that the excess of glutamate could overactivate NMDA receptors on neurons leading to neuronal death. 19 The indirect mechanism of air pollution on both stroke and dementia (especially VD) can be mediated by their effects on cardio-neuro-vascular system by the way of accelerating atherosclerosis, 59 their effects on plaque's formation and rupture, endothelial dysfunctions, cardiac arrhythmia, hypertension, activation of thrombosis.…”

Section: Global Burden Of Diseasementioning

confidence: 99%

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A review of epidemiological research on stroke and dementia and exposure to air pollution

Béjot

Reis

Giroud

et al. 2018

International Journal of Stroke

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Background Outdoor air pollution is now a well-known risk factor for morbidity and mortality, and is increasingly being identified as a major risk factor for stroke. Methods A narrative literature review of the effects of short and long-term exposure to air pollution on stroke and dementia risk and cognitive functioning. Results Ten papers on stroke and 17 on dementia were selected. Air pollution, and in particular small particulate matter, contributes to about one-third of the global stroke burden and about one-fifth of the global burden of dementia. It particularly affects vulnerable patients with other vascular risk factors or a prior history of stroke in low- and medium-income countries. New pathophysiological mechanisms of the cause-effect associations are suggested. Conclusion Air pollution should be considered as a new modifiable cerebrovascular and neurodegenerative risk factor. This massive worldwide public health problem requires environmental health policies able to reduce air pollution and thus the stroke and dementia burden.

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Section: History Of Air Pollutionmentioning

confidence: 99%

Section: Global Burden Of Diseasementioning

confidence: 99%

Section: Global Burden Of Diseasementioning

confidence: 99%

Section: Global Burden Of Diseasementioning

confidence: 99%

Section: Global Burden Of Diseasementioning

confidence: 99%

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A review of epidemiological research on stroke and dementia and exposure to air pollution

Béjot

Reis

Giroud

et al. 2018

International Journal of Stroke

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Investigation of the expression of Cis P‐tau and Pin1 proteins following air pollution induction in the brain tissue of C57BL/6 mice

Shahpasand,

Khatami,

Ehtiati

et al. 2024

Biotech and App Biochem

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Alzheimer's disease (AD) is a multifactorial disease in which environmental factors play a role. Among environmental factors, air pollution is a vital issue in modern life. Despite extensive considerations, it remains uncertain how pollution mediates neurodegeneration in AD. Beta‐amyloids and hyperphosphorylated tau proteins are the two main pathological markers that have been studied in AD so far. Tau protein is basically a phosphoprotein whose functions are controlled by phosphorylation. The function of tau protein is to be located on the surface of microtubules and stabilize them. Studies have shown that phosphorylated tau protein (p‐tau) exists in cis and trans conformations at Thr231, among which cis is highly neurotoxic. The Pin1 enzyme performs the conversion of cis to trans or vice versa. In this study, an experimental mouse model was designed to investigate the formation of cis p‐tau by inducing air pollution. In this way, mice were randomly exposed to pollution at 2‐week, 1‐month, and 2‐month intervals. We investigated the formation of phosphorylated cis tau form during air pollution on mouse brains using Western blots and immunofluorescence. The fluorescent imaging results and Western blotting analysis of mouse brains revealed a significant accumulation of cis p‐tau in pollution‐treated mice models compared to the healthy control mice. According to Western blot results, air pollution induction caused a significant decrease in Pin1 protein. The results clearly show that the tauopathy observed during air pollution is mediated through the formation of cis tau. Our findings unravel tauopathy mysteries upon pollution and would help find a possible therapeutic target to fight the devastating disorder caused by modern life.

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Perinatal diesel exhaust exposure causes persistent changes in the brains of aged mice: An assessment of behavioral and biochemical endpoints related to neurodegenerative disease

Garrick

Cole

Dao

et al. 2023

Environmental Toxicology

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Epidemiological studies support an association between air pollution exposure, specifically particulate matter (PM), and neurodegenerative disease. Diesel exhaust (DE) is a principal component of ambient air pollution and a major contributor of PM. Our study aimed to examine whether early‐life perinatal DE exposure is sufficient to affect behavioral and biochemical endpoints related to Alzheimer's disease later in life. To achieve this, mice were perinatally exposed (embryonic day 0–postnatal day 21) to DE (250–300 μg/m3) or filtered air (FA), and allowed to reach aged status (>18 months). Mice underwent behavioral assessment at 6 and 20 months of age, with tissue collected at 22 months for biochemical endpoints. At 6 months, minimal changes were noted in home‐cage behavior of DE treated animals. At 20 months, an alternation deficit was noted with the T‐maze, although no difference was seen in the object location task or any home‐cage metrics. DE exposure did not alter the expression of Aβ42, phosphorylated tau S199, or total tau. However, IBA‐1 protein, a microglial activation marker, was significantly higher in DE exposed animals. Further, lipid peroxidation levels were significantly higher in the DE exposed animals compared to FA controls. Cytokine levels were largely unchanged with DE exposure, suggesting a lack of inflammation despite persistent lipid peroxidation. Taken together, the findings of this study support that perinatal exposure alone is sufficient to cause lasting changes in the brain, although the effects appear to be less striking than those previously reported in younger animals, suggesting some effects do not persist over time. These findings are encouraging from a public health standpoint and support the aggressive reduction of DE emissions to reduce lifetime exposure and potentially reduce disease outcome.

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Traffic-Related Air Pollution and Neurodegenerative Diseases: Epidemiological and Experimental Evidence, and Potential Underlying Mechanisms

Cited by 9 publications

References 249 publications

A review of epidemiological research on stroke and dementia and exposure to air pollution

A review of epidemiological research on stroke and dementia and exposure to air pollution

Investigation of the expression of Cis P‐tau and Pin1 proteins following air pollution induction in the brain tissue of C57BL/6 mice

Perinatal diesel exhaust exposure causes persistent changes in the brains of aged mice: An assessment of behavioral and biochemical endpoints related to neurodegenerative disease

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