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Inflammation, particularly C-reactive protein (CRP), may mediate these associations, but causal evidence remains limited.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To examine the associations between particulate matter (PM) exposure and cognitive performance, evaluate the causal effects of air pollutants on genetically predicted AD\/ADRD risk using Mendelian randomization (MR), and assess CRP as a potential mediator.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We conducted observational analyses among 7087 older adults from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to evaluate associations between long-term PM exposure and Mini-Mental State Examination (MMSE) scores. Two-sample MR using GWAS summary statistics was performed to estimate the causal effects of PM\n                      <jats:sub>2.5<\/jats:sub>\n                      , PM\n                      <jats:sub>10<\/jats:sub>\n                      , NO\n                      <jats:sub>2<\/jats:sub>\n                      , and NO\n                      <jats:sub>x<\/jats:sub>\n                      on AD risk. Mediation MR assessed CRP's contribution to the PM\u2013AD pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Higher exposure to finer PM was associated with lower MMSE scores, with the strongest associations observed for PM\n                      <jats:sub>1<\/jats:sub>\n                      (\u03b2\u2009=\u2009\u22120.335; 95% CI: \u22120.624 to \u22120.263) and PM\n                      <jats:sub>2.5<\/jats:sub>\n                      (\u03b2\u2009=\u2009\u22120.229; 95% CI: \u22120.367 to \u22120.164). MR analyses identified a causal effect of PM\n                      <jats:sub>10<\/jats:sub>\n                      on AD risk (OR\u2009=\u20091.926; 95% CI: 1.032\u20133.598). CRP mediated 42.9% of this effect (p\u2009=\u20090.003).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Long-term PM exposure, particularly PM\n                      <jats:sub>10<\/jats:sub>\n                      , may contribute to increased AD\/ADRD susceptibility, potentially through inflammation-related pathways. Finer particles showed stronger observational associations with cognitive decline, highlighting the need for further investigation. These findings support air quality improvement and inflammation-targeted strategies for dementia prevention.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251408422","type":"journal-article","created":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T16:55:19Z","timestamp":1767027319000},"page":"1649-1662","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Inflammation as a mediator of air pollution's role in Alzheimer's disease and related dementias"],"prefix":"10.1177","volume":"109","author":[{"given":"Bo","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Neurology &amp; Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chaofan","family":"Geng","sequence":"additional","affiliation":[{"name":"Department of Neurology &amp; 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