{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T02:39:07Z","timestamp":1788316747443,"version":"build-2803163510"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T00:00:00Z","timestamp":1771545600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100022750","name":"Office of the Vice President for Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100022750","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007472","name":"University of Kentucky","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007472","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NIH R01 AG068215"],"award-info":[{"award-number":["NIH R01 AG068215"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Artificial light at night (light pollution) is widespread but understudied in the context of Alzheimer\u2019s disease (AD). Sleep and circadian disruption have been linked to amyloid-\u03b2 (A\u03b2) accumulation and neuroinflammation, but whether dim light at night (dLAN) modifies these processes remains unclear. We tested whether chronic dLAN exposure (8 lux during the dark phase, 8\u00a0weeks) alters circadian rhythms, amyloid pathology, and neuroinflammation in 12\u201313\u00a0month-old humanized APP knock-in (KI) mice. hAPPSAA KI mice, which develop plaques, were compared with hAPPWT KI controls carrying only a humanized APP sequence. dLAN reduced circadian rhythm amplitude and stability while increasing fragmentation in both genotypes within two weeks. In hAPPSAA KI mice, dLAN modestly increased hippocampal plaque burden and soluble neocortical A\u03b2. Astrocyte reactivity was elevated by genotype but not altered by nighttime light exposure. In contrast, microglial markers (CD45, MHCII) were increased with dLAN with CD45+ area elevated in hippocampus, and MHCII+ cell counts greater in the cortex and hippocampus of hAPPSAA KI mice. There were also distinct spatial responses between the microglia markers suggesting that dLAN primes microglia toward an antigen-presenting phenotype (MHCII) in the presence of A\u03b2. Yet, the microglia\/macrophage priming was not associated with amplified cytokine or chemokine levels at the 8-week dLAN exposure timepoint in the brain. These findings add to growing evidence that nighttime light exposure can disrupt circadian and immune regulation, and suggest that environmental light pollution should be further explored as a modifiable factor contributing to Alzheimer\u2019s disease progression.<\/jats:p>","DOI":"10.1093\/sleep\/zsag041","type":"journal-article","created":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T10:41:44Z","timestamp":1771584104000},"source":"Crossref","is-referenced-by-count":3,"title":["Dim light at night impacts circadian rhythms and Alzheimer\u2019s disease-like neuroinflammation and neuropathology in humanized APP SAA knock-in mice"],"prefix":"10.1093","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6298-9016","authenticated-orcid":false,"given":"Marilyn J","family":"Duncan","sequence":"first","affiliation":[{"name":"Department of Neuroscience, University of Kentucky , Lexington, KY ,","place":["United 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