Glial smog: Interplay between air pollution and astrocyte-microglia interactions

Gómez-Budia, Mireia; Konttinen, Henna; Saveleva, Liudmila; Korhonen, Paula; Jalava, Pasi; Malm, Tarja

doi:10.1016/j.neuint.2020.104715

Cited by 33 publications

(25 citation statements)

References 212 publications

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“… 4 Microglia, the resident immune cells of the central nervous system, respond to pollutants and cause inflammatory activation. 28 Activated microglia in animal and cell models exhibit increases in somal size compared with resting microglia. 53 The rN0 reflects diffusion bound within cell membranes in spherical structures less than approximately 10 μm or within multiple cylindrical structures oriented such that diffusion is occurring equally in all directions.…”

Section: Discussionmentioning

confidence: 99%

Association of Outdoor Ambient Fine Particulate Matter With Intracellular White Matter Microstructural Properties Among Children

et al. 2021

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Key Points Question Is annual residential exposure to particulate matter 2.5 μm or less in diameter (PM 2.5 ) associated with neuroimaging diffusion markers of white matter microstructure? Findings This cross-sectional study of 7602 children 9 to 10 years of age found evidence of an association between PM 2.5 exposure and hemispheric differences in white matter microstructure. In hemisphere-specific models, adjusted for confounding variables, statistically significant positive associations were observed between PM 2.5 and restricted isotropic diffusion, and statistically significant negative associations were observed between PM 2.5 and mean diffusivity. Meaning Findings from this study suggest that exposure to PM 2.5 may be associated with differences in white matter microarchitecture, supporting a need for further improvements in air quality to protect the developing brain.

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Section: Discussionmentioning

confidence: 99%

Association of Outdoor Ambient Fine Particulate Matter With Intracellular White Matter Microstructural Properties Among Children

et al. 2021

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“…Cell-based assays have shown that exposure of astrocytes to PM activated janus kinase (JAK)-2/STAT-3 and p38/JNK/ERK pathways in reactive astrocytes triggering iNOS induction and IL-1β production (Li et al, 2016). In this regard, PM has been reported to increase the expression and release of proinflammatory mediators through activation of the NF-κB signaling pathway (Li et al, 1999;Gómez-Budia et al, 2020).…”

Section: Impact On the Dynamics Of Astrocytes And Oligodendrocytesmentioning

confidence: 99%

“…In response to air pollution, microglia are activated through the upregulation of several proinflammatory mediators that affect neuronal function (Gómez-Budia et al, 2020). Microglia respond to air pollution by adopting an amoeboid shape in vitro (Cole et al, 2016;Roqué et al, 2016;Mumaw et al, 2017), as well as in vivo (Araújo et al, 2019).…”

Section: Impact On Microglial Reactivity and Consequences On Neuronsmentioning

confidence: 99%

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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“…Although some effects of air pollution on cells of the olfactory system (main route of entry of UFPs), blood–brain barrier (BBB), and microglia have been studied and summarized [ 12 , 19 ], the effects of UFPs on brain health and function are largely unknown. For example, the BBB limits the entry of harmful substances into the brain parenchyma; however, small and often highly lipophilic molecules of a particular composition can pass through the BBB [ 53 ].…”

Section: Effects Of Traffic-derived Ufps On Brain Health and The Development Of Alzheimer’s Diseasementioning

confidence: 99%

“…Some mechanisms have been revealed. Chronic exposure to complex mixtures of air pollutants in urban environments has been shown to induce toxicological effects in the brain, including chronic inflammation, oxidative stress, loss of protein homeostasis, and disruption of the blood–brain barrier (BBB) [ 16 , 17 , 18 , 19 , 20 ]. Clearance is critical to limit the adverse effects induced by pollutants; however, it is not known how and if solid particles are cleared from the brain.…”

Section: Introductionmentioning

confidence: 99%

TUBE Project: Transport-Derived Ultrafines and the Brain Effects

Martikainen

Aakko-Saksa

Broek

et al. 2021

IJERPH

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The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.

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Glial smog: Interplay between air pollution and astrocyte-microglia interactions

Cited by 33 publications

References 212 publications

Association of Outdoor Ambient Fine Particulate Matter With Intracellular White Matter Microstructural Properties Among Children

Association of Outdoor Ambient Fine Particulate Matter With Intracellular White Matter Microstructural Properties Among Children

Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors

TUBE Project: Transport-Derived Ultrafines and the Brain Effects

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