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These major risk factors of Alzheimer\u2019s disease (AD) were examined in mice given chronic exposure to nPM, a nano-sized subfraction of urban air pollution. In the cerebral cortex, female mice had two-fold more genes responding to nPM than males. Transcriptomic responses to nPM had sex-APOE interactions in AD-relevant pathways. Only APOE3 mice responded to nPM in genes related to Abeta deposition and clearance (Vav2, Vav3, S1009a). Other responding genes included axonal guidance, inflammation (AMPK, NFKB, APK\/JNK signaling), and antioxidant signaling (NRF2, HIF1A). Genes downstream of NFKB and NRF2 responded in opposite directions to nPM. Nrf2 knockdown in microglia augmented NFKB responses to nPM, suggesting a critical role of NRF2 in air pollution neurotoxicity. These findings give a rationale for epidemiologic studies of air pollution to consider sex interactions with APOE alleles and other AD-risk genes.<\/jats:p>","DOI":"10.7554\/elife.54822","type":"journal-article","created":{"date-parts":[[2020,6,24]],"date-time":"2020-06-24T10:00:19Z","timestamp":1592992819000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.54822","source":"Crossref","is-referenced-by-count":37,"title":["Mouse brain transcriptome responses to inhaled nanoparticulate matter differed by sex and APOE in Nrf2-Nfkb interactions"],"prefix":"10.7554","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6052-8793","authenticated-orcid":true,"given":"Amin","family":"Haghani","sequence":"first","affiliation":[{"name":"Leonard Davis School of Gerontology, University of Southern California, Los Angeles, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mafalda","family":"Cacciottolo","sequence":"additional","affiliation":[{"name":"Leonard 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