{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T18:10:24Z","timestamp":1780423824715,"version":"3.54.1"},"reference-count":103,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2024,7,6]],"date-time":"2024-07-06T00:00:00Z","timestamp":1720224000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2024,7,30]]},"abstract":"<jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Neuropsychiatric symptoms (NPS) can be an early manifestation of Alzheimer\u2019s disease (AD). However, the associations among NPS, cognition, and AD biomarkers across the disease spectrum are unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>\n                      We analyzed cross-sectional mediation pathways between cerebrospinal fluid (CSF) biomarkers of AD (A\u03b2\n                      <jats:sub>1-42<\/jats:sub>\n                      , p-tau\n                      <jats:sub>181<\/jats:sub>\n                      ), cognitive function, and NPS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      Primary models included 781 participants from the National Alzheimer\u2019s Coordinating Center (NACC) data set who had CSF analyzed for AD biomarkers using Lumipulse. NPS were assessed with the Neuropsychiatric Inventory Questionnaire (NPI-Q). We assessed cognition with the harmonized MMSE\/MoCA, as well as neuropsychological tests sensitive to AD pathology: story recall, naming, animal fluency, and Trails B. The Clinical Dementia Rating (CDR\n                      <jats:sup>\u00ae<\/jats:sup>\n                      ) scale assessed dementia severity. Mediation models were estimated with Kemeny metric covariance in a structural equation model framework, controlling for age, education, sex, and\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      <jats:italic toggle=\"yes\">\u025b<\/jats:italic>\n                      4.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      The sample was older adults (\n                      <jats:italic toggle=\"yes\">M<\/jats:italic>\n                      \u200a=\u200a73.85,\n                      <jats:italic toggle=\"yes\">SD<\/jats:italic>\n                      \u200a=\u200a6.68; 49.9% male, 390; 27.9% dementia, 218) who were predominantly white (\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      \u200a=\u200a688, 88.1%). Higher p-tau\n                      <jats:sub>181<\/jats:sub>\n                      \/A\u03b2\n                      <jats:sub>1-42<\/jats:sub>\n                      ratio predicted higher NPI-Q, which was partially mediated by the MMSE\/MoCA and, in a second model, story recall. No other pathway was statistically significant. Both the MMSE\/MoCA and NPI-Q independently mediated the association between p-tau\n                      <jats:sub>181<\/jats:sub>\n                      \/A\u03b2\n                      <jats:sub>1-42<\/jats:sub>\n                      ratio and CDR global impairment. With dementia excluded, p-tau\n                      <jats:sub>181<\/jats:sub>\n                      \/A\u03b2\n                      <jats:sub>1-42<\/jats:sub>\n                      ratio was no longer associated with the NPI-Q.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>NPS may be secondary to cognitive impairment and AD pathology through direct and indirect pathways. NPS independently predict dementia severity in AD. However, AD pathology likely plays less of a role in NPS in samples without dementia.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-240125","type":"journal-article","created":{"date-parts":[[2024,7,12]],"date-time":"2024-07-12T10:48:58Z","timestamp":1720781338000},"page":"1055-1073","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":6,"title":["Cognition Mediates the Association Between Cerebrospinal Fluid Biomarkers of Amyloid and P-Tau and Neuropsychiatric Symptoms"],"prefix":"10.1177","volume":"100","author":[{"given":"Brandon","family":"Frank","sequence":"first","affiliation":[{"name":"U.S. Department of Veteran Affairs","place":["USA"]},{"name":"Boston University Chobanian and Avedisian School of Medicine","place":["USA"]},{"name":"Boston University Chobanian and Avedisian School of 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