Exposure to fine particulate matter (PM2.5) hampers myelin repair in a mouse model of white matter demyelination

Parolisi, Roberta; Montarolo, Francesca; Pini, Alessandro; Rovelli, Sabrina; Cattaneo, Andrea; Bertolotto, Antonio; Buffo, Annalisa; Bollati, Valentina; Boda, Enrica

doi:10.1016/j.neuint.2021.104991

Cited by 13 publications

(6 citation statements)

References 22 publications

(25 reference statements)

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“…Based on our results, we could thus infer that higher exposure to PM2.5, PM10 and NO2 can contribute to a worst Covid-19 course also among MS patients. Since a link between air pollutants, including PM2.5, PM10, NO2, and MS was already found ( Bergamaschi et al, 2021 , Tateo et al, 2019 , Noorimotlagh et al, 2021 , Bergamaschi et al, 2018 , Cortese et al, 2020 , Heydarpour et al, 2014 , Gregory et al, 2008 , Parolisi et al, 2021 , Jeanjean et al, 2018 ), it was reasonable to expect that the effects of pollution, widely documented in the general population, would have been confirmed or even further enhanced among MS patients and thus our results are not surprising. Among MS patients, air pollution can thus additionally contribute to the risk of unfavorable Covid-19 course, being a co-factor together with other well known risk factors for the general population (older age, higher BMI and presence of comorbidities) and for patients with MS (higher EDSS, progressive MS phenotype, disease duration and Anti-CD20 treatment).…”

Section: Discussionsupporting

confidence: 69%

The impact of PM2.5, PM10 and NO2 on Covid-19 severity in a sample of patients with multiple sclerosis: A case-control study

Ponzano

Schiavetti

Bergamaschi³

et al. 2022

Multiple Sclerosis and Related Disorders

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Section: Discussionsupporting

confidence: 69%

The impact of PM2.5, PM10 and NO2 on Covid-19 severity in a sample of patients with multiple sclerosis: A case-control study

Ponzano

Schiavetti

Bergamaschi³

et al. 2022

Multiple Sclerosis and Related Disorders

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“…In contrast, more consistent patterns of air pollution-related reduction in total and different associated areas (i.e., frontal, parietal, temporal and corpus callosum) of white matter volumes were reported [60,66,67,68]. Recently, white matter demyelination was also reported in a mouse model with PM 2.5 exposure and was thought to be induced by promoting neuroin ammation or impairing myelin repair [69]. From the results of our study, decreased myelination of the corpus callosum and reduced MBP expression in the white matter of mice exposed to PM 2.5 also support this point of view.…”

Section: Discussionmentioning

confidence: 98%

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Chen

Lee

Zheng

et al. 2021

Preprint

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Background: Air pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially Alzheimer’s disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution. Results: 6-month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract. Conclusions: In conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve is another direct invasion route in addition to olfactory nerve.

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“…Interestingly, females showed significant alterations in oligodendrocytogenesis in the CC (Klocke et al, 2018). Finally, in a mouse model of lysolecithin-induced demyelination of the subcortical white matter, exposure to PM 2.5 hampered remyelination and disrupted oligodendroglia differentiation (Parolisi et al, 2021).…”

Section: Impact On the Dynamics Of Astrocytes And Oligodendrocytesmentioning

confidence: 94%

Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors

Lecordier

Manrique-Castano

Moghrabi

et al. 2021

Front. Aging Neurosci.

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Vascular dementia (VaD) constitutes the second most prevalent cause of dementia in the world after Alzheimer’s disease (AD). VaD regroups heterogeneous neurological conditions in which the decline of cognitive functions, including executive functions, is associated with structural and functional alterations in the cerebral vasculature. Among these cerebrovascular disorders, major stroke, and cerebral small vessel disease (cSVD) constitute the major risk factors for VaD. These conditions alter neurovascular functions leading to blood-brain barrier (BBB) deregulation, neurovascular coupling dysfunction, and inflammation. Accumulation of neurovascular impairments over time underlies the cognitive function decline associated with VaD. Furthermore, several vascular risk factors, such as hypertension, obesity, and diabetes have been shown to exacerbate neurovascular impairments and thus increase VaD prevalence. Importantly, air pollution constitutes an underestimated risk factor that triggers vascular dysfunction via inflammation and oxidative stress. The review summarizes the current knowledge related to the pathological mechanisms linking neurovascular impairments associated with stroke, cSVD, and vascular risk factors with a particular emphasis on air pollution, to VaD etiology and progression. Furthermore, the review discusses the major challenges to fully elucidate the pathobiology of VaD, as well as research directions to outline new therapeutic interventions.

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Exposure to fine particulate matter (PM2.5) hampers myelin repair in a mouse model of white matter demyelination

Cited by 13 publications

References 22 publications

The impact of PM2.5, PM10 and NO2 on Covid-19 severity in a sample of patients with multiple sclerosis: A case-control study

The impact of PM2.5, PM10 and NO2 on Covid-19 severity in a sample of patients with multiple sclerosis: A case-control study

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors

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