Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults

Calderón‐Garcidueñas, Lilian; Solt, Anna C.; Henríquez-Roldán, Carlos; Torres‐Jardón, Ricardo; Nuse, Bryan; Herritt, Lou; Villarreal-Calderón, Rafael; Osnaya, Norma; Stone, Ida M.; Garcı́a, Raquel; Brooks, Diane M.; González-Maciel, Angélica; Reynoso-Robles, Rafael; Delgado‐Chávez, Ricardo; Reed, William

doi:10.1177/0192623307313011

Cited by 789 publications

(683 citation statements)

References 94 publications

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“…This in turn is expected to profoundly impair cytoskeletal stability and axonal integrity and would facilitate the formation of NFTs and senile plaques in affected neurons, thereby tipping the balance from healthy to pathological aging and cognitive deterioration (Krstic and Knuesel, 2013). This view also strongly supports the hypothesis of a pivotal role of olfactory bulb-associated neuroinflammation (Calderon-Garciduenas et al, 2008, Majde, 2010 in the initiation of the late-onset AD.…”

Section: Introductionsupporting

confidence: 53%

“…During the course of aging, however, accumulating injuries to the olfactory system, e.g. by viruses (Majde, 2010) or pollution (Calderon-Garciduenas et al, 2008), may induce excessive neuroinflammation and ultimately lead to well described deterioration of the olfactory system (Lazarini et al, 2012). It is highly conceivable that this in turn will induce pathological changes in relayed brain centers (Koliatsos et al, 2004, Hu et al, 2012.…”

Section: Olfactory-limbic Pathways and Admentioning

confidence: 99%

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Decisive role of Reelin signaling during early stages of Alzheimer’s disease

et al. 2013

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Alzheimer's disease (AD) is one of the largest unmet medical concerns of our society. Around 25 million patients worldwide together with their families are still waiting for an effective treatment. We have recently initiated a re-evaluation of our knowledge of the molecular and cellular mechanisms underlying sporadic AD. Based on the existing literature, we have proposed a mechanistic explanation of how the late-onset form of the disease may evolve on the cellular level. Here, we expand this hypothesis by addressing the pathophysiological changes underlying the early and almost invariant appearance of the neurofibrillary tangles, the only reliable correlate of the cognitive status, in distinct brain areas and their consistent "spread" along interconnected neurons as the disease advances. In this review we present and discuss novel evidence that the extracellular signaling protein Reelin, expressed along the olfactory and limbic pathways in the adult brain, might hold a key to understand the earliest steps of the disease, highlighting the olfactory pathway as the brain's Achilles heel involved in the initiation of the pathophysiological characteristic of late-onset AD. AbstractAlzheimer`s disease (AD) is one of the largest unmet medical needs of our society. Around 25 million patients worldwide together with their families are still waiting for an effective treatment. We have recently initiated a re-evaluation of our knowledge of the molecular and cellular mechanisms underlying sporadic AD. Based on the existing literature, we have proposed a mechanistic explanation of how the late-onset form of the disease may evolve on the cellular level. Here, we expand this hypothesis by addressing the pathophysiological changes underlying the early and almost invariant appearance of the neurofibrillary tangles (NFTs), the only reliable correlate of the cognitive status, in distinct brain areas and their consistent "spread" along interconnected neurons as the disease advances. In this review we present and discuss novel evidence that the extracellular signaling protein Reelin, expressed along the olfactory and limbic pathways in the adult brain, might hold a key to understand the earliest steps of the disease, highlighting the olfactory pathway as the brain's Achilles heel involved in the initiation of the pathophysiology characteristic of late-onset AD.3

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Section: Introductionsupporting

confidence: 53%

Section: Olfactory-limbic Pathways and Admentioning

confidence: 99%

Decisive role of Reelin signaling during early stages of Alzheimer’s disease

et al. 2013

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“…It has been shown that chronic exposure to urban air pollution can lead to disruption of the blood-brain barrier, endothelial activation, and enhanced inflammatory status of the brain. 53 Second, high LDL levels have not been shown as an independent risk factor for IS in contrast to their high impact on cardiovascular outcomes. 54 However, the PMdriven acceleration of arterial plaque burden is maintained by LDL.…”

Section: Perspectives On Neurovascular Researchmentioning

confidence: 99%

Impact of Particulate Matter Exposition on the Risk of Ischemic Stroke: Epidemiologic Evidence and Putative Mechanisms

Bornstädt

Kunz

Endres

2013

J Cereb Blood Flow Metab

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Ambient particulate matter (PM) pollution is estimated to be responsible for 3.2 million deaths annually worldwide. Although many studies have demonstrated PM as a serious risk factor for cardiovascular diseases, less is known on its association with cerebrovascular events. Over the last decade, however, an increasing number of studies have provided data showing a relationship between PM exposure and ischemic stroke (IS). In this article, we will report on existing epidemiologic findings for an association between PM exposure and IS based on a systemic literature search. Thus, despite inconsistencies in the results, currently available data suggest that PM exposure is a risk factor for IS, especially in patients with preexisting illnesses. With regards to the mechanisms leading to PM-dependent vascular damage, in particular proinflammatory, prooxidative, as well as proatherogenic pathways have been suggested to be involved. Notably, to date there is only one study published, which demonstrates the influence of PM exposure on cerebrovascular function. We will discuss reasonable approaches for future neurovascular research in this field.

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“…Chronic exposure has shown to cause epithelium and respiratory alterations2 leading to other chronic health outcomes including nonfatal heart attacks,3 stroke,4 asthma,5, 6 and decreased lung function 7, 8. Fine particulate matter (PM 2.5 ) has also been associated with adverse neurological outcomes including cognitive delays in children,9, 10, 11 dementia and Alzheimers,12, 13, 14 and white matter abnormalities 14, 15, 16. Animal studies show that long‐term exposure to PM 2.5 can decrease total brain and white matter volumes 17…”

Section: Introductionmentioning

confidence: 99%

Urban air quality and associations with pediatric multiple sclerosis

Lavery

Waubant

Casper

et al. 2018

Ann Clin Transl Neurol

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BackgroundWe previously identified air quality as a risk factor of interest for pediatric multiple sclerosis. The purpose of this study is to more closely examine the association between the six criteria air pollutants and pediatric MS as well as identify specific areas of toxic release using data from the Toxic Release Inventory.MethodsPediatric MS cases (N = 290) and healthy controls (N = 442) were included as part of an ongoing case–control study. We used the National Emissions Inventory system to estimate particulate exposure by county of residence for each participant. Proximity to Toxic Release Inventory (TRI) sites was also assessed using ArcGIS mapping tools. Risk‐Screening Environmental Indicators (RSEI) classified counties at risk to exposure of environmental toxic releases.ResultsFine particulate matter (PM 2.5), carbon monoxide (CO), sulfur dioxide (SO 2), and lead air emissions were associated with increased odds for pediatric MS (P < 0.01) for those residing within 20 miles of an MS center. Most study participants (75%) resided within 5 miles of at least one TRI site; however, the mean total pounds of stack air releases was higher for sites near MS cases (81,000 tons) compared to those near healthy controls (35,000 tons, P = 0.002). Average RSEI scores did not differ significantly between cases and controls.ConclusionOut of several air pollutants examined, we show that fine particulate matter and three other criteria pollutants (SO 2, CO, and lead) were statistically associated with higher odds for pediatric MS.

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Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults

Cited by 789 publications

References 94 publications

Decisive role of Reelin signaling during early stages of Alzheimer’s disease

Decisive role of Reelin signaling during early stages of Alzheimer’s disease

Impact of Particulate Matter Exposition on the Risk of Ischemic Stroke: Epidemiologic Evidence and Putative Mechanisms

Urban air quality and associations with pediatric multiple sclerosis

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