NEUROTOXIC EFFECTS OF AMBIENT AIR POLLUTION ON BRAIN STRUCTURE AND DEMENTIA RISK IN OLDER WOMEN

AIR POLLUTION IN BRAIN AGING AND DEMENTIA Chair: C.E. Finch, University Southern California, Los Angeles, California Co-Chair: J. Chen, University of Southern California, Los Angeles, California Discussant: G.M. Martin, University of Washington Over 75% of older Americans are living in metropolitan areas, and this urban-dwelling aging population will continue to grow in the coming decades. Ambient air pollution, a ubiquitous exposure in urban environments, has emerged as a new environmental factor in brain aging and dementia. Over the last few years, accumulating epidemiologic and neurotoxicological data have shown the aging brain is vulnerable to neurotoxic effects of ambient air pollutants. For instance, elevated levels of fine particulate matter (PM2.5: PM with aerodynamic diameters<2.5μm) are associated with several years of faster cognitive aging and loss of white matter volume. Rodent brain models with inhaled PM exposure suggest the neurodegenerative mechanisms may involve increased neuroinflammation and soluble amyloid, and attrition of glutamate receptors. Assembling four presentations with new findings, this symposium aims to better define the individual risk, heterogeneity, and pathobiological mechanisms linking ambient air pollutants with brain aging and dementia. Epidemiological studies show that both PM2.5 and O3 exposures may increase the risk for dementia in older women (Chen). Epidemiologic studies also show that PM2.5 –associated adverse effects on aging brain may be strengthened in populations with APOE4 alleles (Chen) and in populations of low educational attainment (Ailshire). Rodent models with PM exposures from traffic emissions document the role of the lung-brain axis in microglial activation (Block) and illustrate ApoE4 interaction with exposure contributing to brain amyloid deposition (Cacciottolo). Together these findings show that environmental factors contribute to accelerated brain aging in synergy with the ApoE4 allele risk factor for Alzheimer disease.