10th International Aerosol Conference
September 2 - September 7, 2018
America's Center Convention Complex
St. Louis, Missouri, USA

Abstract View


Near-Roadway Effects on the Progression of Alzheimer’s Disease

KEITH BEIN, Christopher Wallis, Xiao-San Luo, Kelley Patten, Anthony Valenzuela, Elizabeth Berg, Jill Silverman, Pamela Lein, Anthony S. Wexler, University of California Davis

     Abstract Number: 636
     Working Group: Aerosol Exposure

Abstract
Recent epidemiological studies have linked traffic-related air pollution (TRAP) to increased risk of Alzheimer’s disease (AD). In addition, in vivo and in vitro studies have shown that individual components of TRAP can alter neuroinflammation, increase neurotransmitter levels, and increase neurogenesis. However, TRAP exposures are challenging to reproduce in laboratory settings, and the mechanisms by which TRAP leads to Alzheimer’s-related cognitive deficits remain unclear. To address these issues, we exposed male and female wildtype and transgenic Fischer 344 (TgF344-AD) rats to real-time TRAP, using an exposure facility that samples air directly from a highway tunnel in the Bay Area of California used by both light- and heavy-duty vehicles. TRAP and filtered air (FA) PM samples were collected for 24 hours once every third day, and a subset of these were analyzed for particulate matter mass, organic and elemental carbon composition, and elemental composition. Gas phase samples were collected monthly on sorbents and analyzed for molecular organics. The goal of this project is to test the hypotheses that exposure to TRAP triggers inflammatory responses in the brain that initiate, accelerate or exacerbate progressive AD pathology and cognitive dysfunction, and that the response to TRAP varies depending upon sex, age, and expression of AD susceptibility genes. To test these hypotheses, we are quantifying cytokines in the periphery and brain, neuroinflammation, neuropathology, and cognitive impairment in rats genetically predisposed to AD and their wildtype littermates exposed to TRAP or FA beginning at postnatal day 28.

This work was supported by the NIEHS (grants R21 ES026515 and P30 ES023513), NIA (grant P30AG010129), NICHD (grant U54 HD079125) and NIMH (T32 MH112507).