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Background: The potential effect of the antiplatelet and anti-inflammatory properties of aspirin on Alzheimer's disease development, especially its role in the progression from mild cognitive impairment to Alzheimer's disease dementia, remains controversial. To evaluate the association between aspirin, use and the risk of conversion to Alzheimer's disease dementia among individuals diagnosed with mild cognitive impairment.
Methods: In this retrospective population-based cohort study, we used the Korean National Health Insurance Service database to collect data on patients with mild cognitive impairment enrolled between 2013 and 2016 and followed up until 2021. In total, 508,107 patients initially diagnosed with mild cognitive impairment (192,538 with aspirin prescriptions and 315,569 without aspirin prescriptions) were enrolled. Aspirin use was assessed by extracting information from the Korean National Health Insurance Service database using aspirin prescription codes. The primary outcome was newly diagnosed Alzheimer's disease dementia. Hazard ratios and 95% confidence intervals for Alzheimer's disease were analyzed according to aspirin use using Cox proportional hazards regression analysis. Secondary outcomes included ischemic and hemorrhagic stroke risk associated with aspirin use.
Results: The data of 508,107 individuals were analyzed (mean [standard deviation] age, 67.6 [10.7] years; 66.8% women and 33.2% men), and 39,318 developed Alzheimer's disease (22,572 controls and 16,746 using aspirin). The rate of conversion to Alzheimer's disease was lower in the aspirin user group, and the time to Alzheimer's disease dementia occurrence was longer than in the nonuser group. A decreased Alzheimer's disease dementia risk was found in patients using aspirin in Model 2 (adjusted hazard ratio, 0.939; 95% confidence interval, 0.920-0.959), with more pronounced effects in individuals aged ≥65 years (Model 2 adjusted hazard ratio, 0.934; 95% confidence interval, 0.914-0.955). For hemorrhagic stroke, the risk increased with aspirin use across all age groups, with the highest risk observed in younger patients (Model 2 adjusted hazard ratio, 5.082; 95% confidence interval, 4.838-5.338).
Conclusion: Aspirin use was associated with reduced Alzheimer's disease risk in older patients with mild cognitive impairment. Notably, the bleeding risk associated with aspirin use should be considered, and personalized treatment should be provided.
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http://dx.doi.org/10.3389/fnagi.2025.1603892 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Institute of Cardiovascular Diseases and Department of Cardiology, Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu (K.L., H.M., W.J
Background: The estimated glucose disposal rate (eGDR) is a validated surrogate marker of insulin resistance. However, its association with stroke and dementia in nondiabetic populations remains insufficiently investigated.
Methods: This prospective cohort study included nondiabetic participants from the UK Biobank.
Lab Chip
September 2025
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Traumatic brain injuries (TBIs) are a risk factor for Alzheimer's disease (AD), and share several important pathological features including the development of neurofibrillary tangles (NFT) of tau protein. While this association is well established, the underlying pathogenesis is poorly defined and current treatment options remain limited, necessitating novel methods and approaches. In response we developed "TBI-on-a-chip", an trauma model utilizing murine cortical networks on microelectrode arrays (MEAs), capable of reproducing clinically relevant impact injuries while providing simultaneous morphological and electrophysiological readout.
View Article and Find Full Text PDFJ Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFJ Neuropsychiatry Clin Neurosci
September 2025
Departments of Psychiatry and Neurology, Center for Brain/Mind Medicine, and Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston.
Neuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDF