{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:00:32Z","timestamp":1789970432554,"version":"4.0.1"},"reference-count":69,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:00:00Z","timestamp":1789948800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontierspartnerships.org"],"crossmark-restriction":true},"short-container-title":["Br. J. Biomed. Sci."],"abstract":"<jats:p>\n                    Alzheimer\u2019s disease (AD) is characterized by progressive cognitive decline, amyloid-\u03b2 and tau aggregation, and chronic neuroinflammation, processes that are tightly coupled to circadian and metabolic dysfunction. REV-ERB\u03b1 (NR1D1) and REV-ERB\u03b2 (NR1D2) are ligand-dependent nuclear receptors that function as transcriptional repressors within the core clock and coordinate programs governing lipid metabolism, innate immunity, and redox homeostasis in the brain. In microglia, REV-ERB\u03b1 restrains NF-\u03baB signaling, complement and inflammasome activation, and lipid droplet accumulation, thereby limiting synaptic engulfment and tauopathy progression, whereas its loss drives a hyper-reactive, neurotoxic state. Astrocytic REV-ERB\u03b1 exerts context-dependent effects, simultaneously constraining cytokine and nitric oxide production while tuning NAD\n                    <jats:sup>+<\/jats:sup>\n                    metabolism through an NFIL3\u2013CD38 axis with implications for tau-induced neurodegeneration. Preclinical studies demonstrate that synthetic pan-REV-ERB agonists reduce glial activation, restore NCoR\/HDAC3-mediated repression, improve cognitive performance, and partially realign disrupted circadian rhythms in AD models, although current compounds are limited by suboptimal pharmacokinetics and off-target actions. In this narrative review, REV-ERBs are presented as nodal integrators of circadian, metabolic, and neuroimmune pathways in AD and as promising, yet complex, therapeutic targets, highlighting opportunities for brain-penetrant ligands, rational combinations, and chronotherapeutic dosing paradigms.\n                  <\/jats:p>","DOI":"10.3389\/bjbs.2026.16121","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T05:10:15Z","timestamp":1789967415000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["REV-ERBs as regulators of circadian rhythm, neuroinflammation, and glial lipid homeostasis in Alzheimer\u2019s disease. A narrative review"],"prefix":"10.3389","volume":"83","author":[{"given":"Fahmida","family":"Shabnam","sequence":"first","affiliation":[{"name":"Department of Anatomy, Physiology and Pharmacology, Auburn University College of Veterinary Medicine","place":["Auburn, AL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meenakshi","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery, Auburn University Harrison College of Pharmacy","place":["Auburn, AL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajesh","family":"Amin","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery, Auburn University Harrison College of Pharmacy","place":["Auburn, AL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristine","family":"Griffett","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Physiology and Pharmacology, Auburn 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