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Due to a significant increase in the global burden of diabetes and population ageing, DACD is becoming an important public health issue. This review provides a comprehensive overview of the pathophysiology, molecular mechanisms, biomarkers, experimental models, and emerging therapeutic strategies associated with DACD. At present, it is believed that the multiple mechanisms associated with chronic hyperglycemia, insulin resistance, oxidative stress, mitochondrial dysfunction, neuroinflammation, blood\u2013brain barrier disruption, and microvascular injury all contribute to the pathogenesis of DACD. These interrelated mechanisms are responsible for cognitive decline, synaptic dysfunction, and neuronal damage. Experimental research has shown that specific molecular pathways contribute to the pathogenesis of DACD, such as AGE\u2013RAGE signaling, nuclear factor-\u03baB activation, PI3K\/Akt dysregulation, and inflammatory cascades. Emerging biomarkers including neurofilament light (NfL) chain, phosphorylated tau (p-tau), neuroimaging markers, exosomes, metabolomic profiles, and transcriptomic signatures may improve early diagnosis and risk stratification. Several therapeutic approaches, including GLP-1 receptor agonists, SGLT2 inhibitors, DPP-4 inhibitors, intranasal insulin, nanoparticle-based delivery systems, stem cell therapies, and bioactive compounds, have demonstrated promising neuroprotective effects in preclinical studies, although clinical translation remains limited. Finally, future studies should be directed toward the use of biomarker-driven diagnosis, clinically relevant disease models, and large-scale clinical studies in order to develop effective therapeutic interventions. Understanding more of the mechanisms that underlie DACD could help inform the creation of precision medicine strategies to prevent or delay diabetes-related cognitive decline.<\/jats:p>","DOI":"10.1021\/acsptsci.6c00440","type":"journal-article","created":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:02:21Z","timestamp":1790773341000},"page":"2688-2711","source":"Crossref","is-referenced-by-count":0,"title":["Diabetes-Associated\nCognitive Dysfunction: Pathophysiology,\nMolecular Mechanisms, and Emerging Therapeutic Strategies"],"prefix":"10.1021","volume":"9","author":[{"given":"Ravin","family":"Sarkar","sequence":"first","affiliation":[{"name":"Chandigarh University , , , ,","place":["Gharuan, Punjab, India, 140413"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2890-1575","authenticated-orcid":true,"given":"Atul","family":"Kabra","sequence":"additional","affiliation":[{"name":"Chandigarh University , , , ,","place":["Gharuan, Punjab, India, 140413"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdulaziz","family":"S. Saeedan","sequence":"additional","affiliation":[{"name":"Prince Sattam Bin Abdulaziz University , , ,","place":["Al-Kharj, Saudi Arabia, 16273"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8580-3002","authenticated-orcid":true,"given":"Mohd Nazam","family":"Ansari","sequence":"additional","affiliation":[{"name":"Prince Sattam Bin Abdulaziz University , , ,","place":["Al-Kharj, Saudi Arabia, 16273"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"316","published-online":{"date-parts":[[2026,9,30]]},"reference":[{"key":"2026100909100076500_cit1","doi-asserted-by":"publisher","first-page":"20241091","DOI":"10.1515\/med-2024-1091","article-title":"Diabetes-related cognitive impairment:\nMechanisms, symptoms, and treatments","volume":"20","author":"Yu","year":"2025","journal-title":"Open Med."},{"issue":"1","key":"2026100909100076500_cit2","doi-asserted-by":"publisher","first-page":"14688","DOI":"10.1038\/s41598-025-99606-4","article-title":"Metabolomic signatures\nof cognitive function in a type 2 Diabetes-Enriched cohort","volume":"15","author":"Powell","year":"2025","journal-title":"Sci. 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