{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T06:58:31Z","timestamp":1793257111348,"version":"4.5.0"},"reference-count":110,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2022,6,7]],"date-time":"2022-06-07T00:00:00Z","timestamp":1654560000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,9,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Study Objectives<\/jats:title>\n                  <jats:p>Fast frequency sleep spindles are reduced in aging and Alzheimer\u2019s disease (AD), but the mechanisms and functional relevance of these deficits remain unclear. The study objective was to identify AD biomarkers associated with fast sleep spindle deficits in cognitively unimpaired older adults at risk for AD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Fifty-eight cognitively unimpaired, \u03b2-amyloid-negative, older adults (mean\u2005\u00b1\u2005SD; 61.4\u2005\u00b1\u20056.3 years, 38 female) enriched with parental history of AD (77.6%) and apolipoprotein E (APOE) \u03b54 positivity (25.9%) completed the study. Cerebrospinal fluid (CSF) biomarkers of central nervous system inflammation, \u03b2-amyloid and tau proteins, and neurodegeneration were combined with polysomnography (PSG) using high-density electroencephalography and assessment of overnight memory retention. Parallelized serial mediation models were used to assess indirect effects of age on fast frequency (13 to &amp;lt;16Hz) sleep spindle measures through these AD biomarkers.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Glial activation was associated with prefrontal fast frequency sleep spindle expression deficits. While adjusting for sex, APOE \u03b54 genotype, apnea\u2013hypopnea index, and time between CSF sampling and sleep study, serial mediation models detected indirect effects of age on fast sleep spindle expression through microglial activation markers and then tau phosphorylation and synaptic degeneration markers. Sleep spindle expression at these electrodes was also associated with overnight memory retention in multiple regression models adjusting for covariates.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>These findings point toward microglia dysfunction as associated with tau phosphorylation, synaptic loss, sleep spindle deficits, and memory impairment even prior to \u03b2-amyloid positivity, thus offering a promising candidate therapeutic target to arrest cognitive decline associated with aging and AD.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/sleep\/zsac135","type":"journal-article","created":{"date-parts":[[2022,6,7]],"date-time":"2022-06-07T09:39:56Z","timestamp":1654594796000},"source":"Crossref","is-referenced-by-count":64,"title":["Inflammation, tau pathology, and synaptic integrity associated with sleep spindles and memory prior to \u03b2-amyloid positivity"],"prefix":"10.1093","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0831-7980","authenticated-orcid":false,"given":"Bryce A","family":"Mander","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Human Behavior, University of California , Irvine, CA , USA"},{"name":"Center for the Neurobiology of Learning and Memory, University of California , Irvine, CA , USA"},{"name":"Department of Cognitive Sciences, University of California, Irvine , CA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abhishek","family":"Dave","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Human Behavior, University of California , Irvine, CA , USA"},{"name":"Department of Cognitive Sciences, University of California, Irvine , CA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7586-0118","authenticated-orcid":false,"given":"Kitty 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S. Middleton Veterans Hospital , Madison, WI , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ozioma C","family":"Okonkwo","sequence":"additional","affiliation":[{"name":"Wisconsin Alzheimer\u2019s Disease Research Center, University of Wisconsin-Madison , Madison, WI , USA"},{"name":"Wisconsin Alzheimer\u2019s Institute , Madison, WI , USA"},{"name":"Geriatric Research Education and Clinical Center, Wm. S. Middleton Veterans Hospital , Madison, WI , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay","family":"Asthana","sequence":"additional","affiliation":[{"name":"Wisconsin Alzheimer\u2019s Disease Research Center, University of Wisconsin-Madison , Madison, WI , USA"},{"name":"Wisconsin Alzheimer\u2019s Institute , Madison, WI , USA"},{"name":"Geriatric Research Education and Clinical Center, Wm. S. 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