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This narrative review synthesizes recent literature on how circadian dysfunction may contribute to AD pathogenesis, biomarker profiles, and treatment response. Mechanistic studies suggest important interactions between core clock genes and neurodegenerative cascades involving oxidative stress, neuroinflammation, glial reactivity, and proteostasis. Disruptions in circadian\u2010regulated molecular pathways, including brain and muscle ARNT\u2010like 1 (\n                    <jats:italic>BMAL1<\/jats:italic>\n                    )\u2013sirtuin 1 (\n                    <jats:italic>SIRT1<\/jats:italic>\n                    ), nuclear factor kappa B (\n                    <jats:italic>NF\u2010\u03baB<\/jats:italic>\n                    )\u2013NOD\u2010like receptor family pyrin domain containing 3 (\n                    <jats:italic>NLRP3<\/jats:italic>\n                    ), and period circadian regulator 2 (\n                    <jats:italic>PER2<\/jats:italic>\n                    )\u2013antioxidant signaling pathways, may compromise neuronal resilience and worsen AD\u2010related pathology. Emerging evidence also suggests distinct circadian patterns in AD\u2010relevant biomarkers, including melatonin, cortisol, orexin, core body temperature, blood\u2013brain barrier permeability, and glial marker oscillations. These rhythmic patterns may have diagnostic and prognostic relevance and support the need for time\u2010aware biomarker interpretation. Chronotherapeutic strategies targeting circadian biology, including melatonin receptor agonists, light therapy, time\u2010restricted feeding, and circadian\u2010aligned drug delivery systems, may help improve targeted clinical endpoints in AD. This review also discusses chronoepigenetics as an emerging area in which clock\u2010regulated epigenetic modifications may influence neurodegenerative trajectories. Future directions include next\u2010generation chronotherapeutic targets, such as glial clocks, clock\u2010gated inflammatory mechanisms, and systemic comorbidities with circadian modulation, including diabetes and hypertension. Overall, the available evidence supports a close association between circadian disruption and both AD pathology and therapeutic response, while also highlighting important gaps in large\u2010scale clinical trials. This time\u2010oriented perspective may support the development of personalized, biomarker\u2010guided, and rhythm\u2010informed approaches to AD care. By bridging chronobiology and neurodegeneration, this review highlights how circadian precision medicine may refine future approaches to understanding and managing AD.\n                  <\/jats:p>","DOI":"10.1002\/nep3.70046","type":"journal-article","created":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T14:46:21Z","timestamp":1784213181000},"page":"229-247","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Circadian rhythms and chronotherapy in Alzheimer's disease: Mechanisms and therapeutic implications"],"prefix":"10.1002","volume":"4","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1395-4095","authenticated-orcid":false,"given":"Bivek","family":"Singh","sequence":"first","affiliation":[{"name":"Department of Neurology Shanghai East Hospital, Tongji University School of Medicine Shanghai China"},{"name":"International Medical School and Postgraduate Centre Management and Science University Shah Alam 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