| Sign In to gain access to subscriptions and/or personal tools. |
DOI: 10.1080/01926230490520232 Brain Inflammation and Alzheimer's-Like Pathology in Individuals Exposed to Severe Air PollutionInstituto Nacional de Pediatría, Mexico City 14410, Mexico, Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, NC 27599-7525, USA
Department of Pediatrics and Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, 27599-7310, USA
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Departamento de Estadística, Universidad de Valparaíso, Chile
Pathology Department, Instituto Nacional de Cancerología, Mexico City, Mexico
Hospital de Especialidades No. 25, and Centro de Investigación Biomédica del Noreste CIBIN, IMSS, Monterrey, NL, Mexico
Hospital de Especialidades No. 25, IMSS, Monterrey, NL, Mexico
Escuela Médico Militar, Universidad del Ejército y Fuerza Aérea, Mexico City, Mexico
Departamento de Patología, Hospital Central Militar, Mexico City, Mexico
Facultad de Medicina, NUCE, Universidad Nacional Autónoma de México, Mexico City, Mexico
Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, NC 27599-7525, USA
Centro de Ciencias de la Atmósfera, Universidad Nacional Autónoma de México, Mexico City, Mexico
Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, NC 27599-7525, USA, Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, NC 27599-7431, USA, james_swenberg{at}unc.edu
Air pollution is a complex mixture of gases (e.g., ozone), particulate matter, and organic compounds present in outdoor and indoor air. Dogs exposed to severe air pollution exhibit chronic inflammation and acceleration of Alzheimer's-like pathology, suggesting that the brain is adversely affected by pollutants. We investigated whether residency in cities with high levels of air pollution is associated with human brain inflammation. Expression of cyclooxygenase-2 (COX2), an inflammatory mediator, and accumulation of the 42-amino acid form of β-amyloid (Aβ42), a cause of neuronal dysfunction, were measured in autopsy brain tissues of cognitively and neurologically intact lifelong residents of cities having low (n:9) or high (n:10) levels of air pollution. Genomic DNA apurinic/apyrimidinic sites, nuclear factor-
Key Words: Brain • β-amyloid • cyclooxygenase 2 • inflammation • neuropathology • air pollution • Mexico City.
This article has been cited by other articles:
|
||||||||||||||||||||||||||||||||||||||||||||||||
 |
|
|
 |
|
Sign In to gain access to subscriptions and/or personal tools.
B activation and apolipoprotein E genotype were also evaluated. Residents of cities with severe air pollution had significantly higher COX2 expression in frontal cortex and hippocampus and greater neuronal and astrocytic accumulation of Aβ42 compared to residents in low air pollution cities. Increased COX2 expression and Aβ42 accumulation were also observed in the olfactory bulb. These findings suggest that exposure to severe airpollution is associated with brain inflammation and Aβ 42 accumulation, two causes of neuronal dysfunction that precede the appearance of neuritic plaques and neurofibrillary tangles, hallmarks of Alzheimer's disease. 
