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Lilian Calder?n-Garcidue?as, Maricela Franco-Lira, Antonieta Mora-Tiscare?o, Humberto Medina-Cortina, Ricardo Torres-Jard?n, and Michael Kavanaugh, “Early Alzheimer’s and Parkinson’s Disease Pathology in Urban Children: Friend versus Foe Responses—It Is Time to Face the Evidence,” BioMed Research International, vol. 2013, Article ID 161687, 16 pages, 2013. doi:10.1155/2013/161687
Copyright ? 2013 Lilian Calder?n-Garcidue?as et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Chronic exposure to particulate matter air pollution is known to cause inflammation leading to respiratory- and cardiovascular-related sickness and death. Mexico City Metropolitan Area children exhibit an early brain imbalance in genes involved in oxidative stress, inflammation, and innate and adaptive immune responses. Early dysregulated neuroinflammation, brain microvascular damage, production of potent vasoconstrictors, and perturbations in the integrity of the neurovascular unit likely contribute to progressive neurodegenerative processes. The accumulation of misfolded proteins coincides with the anatomical distribution observed in the early stages of both Alzheimer’s and Parkinson's diseases. We contend misfolding of hyperphosphorylated tau (HPπ), alpha-synuclein, and beta-amyloid could represent a compensatory early protective response to the sustained systemic and brain inflammation. However, we favor the view that the chronic systemic and brain dysregulated inflammation and the diffuse vascular damage contribute to the establishment of neurodegenerative processes with childhood clinical manifestations. Friend turns Foe early; therefore, implementation of neuroprotective measures to ameliorate or stop the inflammatory and neurodegenerative processes is warranted in exposed children. Epidemiological, cognitive, structural, and functional neuroimaging and mechanistic studies into the association between air pollution exposures and the development of neuroinflammation and neurodegeneration in children are of pressing importance for public health.
1. Introduction
Air pollution is a significant health problem in megacities around the world [1–3]. In a scenario where the projected world population will have a further increase of 2 to 4.5 billion in the first 50 years of this century [4], the issue of deteriorating environments and their health impact is critical. The problem of air pollution is not confined to large urban centers, it also affects small cities and rural areas. Particulate matter (PM) air pollution is a public health problem affecting millions of people worldwide.
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Summary
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We have a 50-year window of opportunity between the early brain changes observed in children and the time when the patient with mild cognitive impairment or dementia will show up at the neurologist’s door. Facing the current pediatric clinical and pathology evidence is imperative if we are aiming our efforts to identify and mitigate environmental factors that influence AD and PD pathogenesis.
One thing is clear: early implementation of neuroprotective measures to ameliorate or stop the inflammatory and neurodegenerative processes in children is warranted [43, 87]. Identification of biomarkers associating systemic inflammation to brain growth is also critical for detecting children at higher risk for cognitive deficits and neurodegeneration.
It is important to remember there is a severe and woeful deficit of progress in the development of both AD and PD-modifying therapy [127, 128]. Since fine and ultrafine PM likely play a key role in the development of neuroinflammation and neurodegeneration, it is very noteworthy that in the US alone, as of December 2012, more than 74 million people are being exposed to concentrations of PM2.5 above the 2006 standards (PM2.5 annual standard of 15 μg/m3) [129]. An appeal to research supporting institutions may be made to strongly invest in defining the CNS pathology associated with exposure to air pollutants in children and young adults and as Castellani and Perry suggested, consider a systems biology approach and an early preventive pathway [128].
Epidemiological, cognitive, and mechanistic studies into the association between air pollution exposures and the development of CNS damage in children are of pressing importance for public health and quality of life. ...
Copyright ? 2013 Lilian Calder?n-Garcidue?as et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Chronic exposure to particulate matter air pollution is known to cause inflammation leading to respiratory- and cardiovascular-related sickness and death. Mexico City Metropolitan Area children exhibit an early brain imbalance in genes involved in oxidative stress, inflammation, and innate and adaptive immune responses. Early dysregulated neuroinflammation, brain microvascular damage, production of potent vasoconstrictors, and perturbations in the integrity of the neurovascular unit likely contribute to progressive neurodegenerative processes. The accumulation of misfolded proteins coincides with the anatomical distribution observed in the early stages of both Alzheimer’s and Parkinson's diseases. We contend misfolding of hyperphosphorylated tau (HPπ), alpha-synuclein, and beta-amyloid could represent a compensatory early protective response to the sustained systemic and brain inflammation. However, we favor the view that the chronic systemic and brain dysregulated inflammation and the diffuse vascular damage contribute to the establishment of neurodegenerative processes with childhood clinical manifestations. Friend turns Foe early; therefore, implementation of neuroprotective measures to ameliorate or stop the inflammatory and neurodegenerative processes is warranted in exposed children. Epidemiological, cognitive, structural, and functional neuroimaging and mechanistic studies into the association between air pollution exposures and the development of neuroinflammation and neurodegeneration in children are of pressing importance for public health.
1. Introduction
Air pollution is a significant health problem in megacities around the world [1–3]. In a scenario where the projected world population will have a further increase of 2 to 4.5 billion in the first 50 years of this century [4], the issue of deteriorating environments and their health impact is critical. The problem of air pollution is not confined to large urban centers, it also affects small cities and rural areas. Particulate matter (PM) air pollution is a public health problem affecting millions of people worldwide.
...
Summary
...
We have a 50-year window of opportunity between the early brain changes observed in children and the time when the patient with mild cognitive impairment or dementia will show up at the neurologist’s door. Facing the current pediatric clinical and pathology evidence is imperative if we are aiming our efforts to identify and mitigate environmental factors that influence AD and PD pathogenesis.
One thing is clear: early implementation of neuroprotective measures to ameliorate or stop the inflammatory and neurodegenerative processes in children is warranted [43, 87]. Identification of biomarkers associating systemic inflammation to brain growth is also critical for detecting children at higher risk for cognitive deficits and neurodegeneration.
It is important to remember there is a severe and woeful deficit of progress in the development of both AD and PD-modifying therapy [127, 128]. Since fine and ultrafine PM likely play a key role in the development of neuroinflammation and neurodegeneration, it is very noteworthy that in the US alone, as of December 2012, more than 74 million people are being exposed to concentrations of PM2.5 above the 2006 standards (PM2.5 annual standard of 15 μg/m3) [129]. An appeal to research supporting institutions may be made to strongly invest in defining the CNS pathology associated with exposure to air pollutants in children and young adults and as Castellani and Perry suggested, consider a systems biology approach and an early preventive pathway [128].
Epidemiological, cognitive, and mechanistic studies into the association between air pollution exposures and the development of CNS damage in children are of pressing importance for public health and quality of life. ...