NOAC Use Linked to Slower Cognitive Decline in New Study

A nationwide Swedish observational study suggests use of non–vitamin K antagonist oral anticoagulants (NOACs) may be associated with slower cognitive decline among patients with atrial fibrillation (AF) and established Alzheimer disease. The findings also linked NOAC treatment to lower risks of several adverse clinical outcomes compared with no anticoagulation.¹

“There are reasons to believe that the treatment could have a positive effect on cognition, for example by improving blood flow and reducing small-scale damage in the brain,” lead author Maria Eriksdotter, MD, PhD, professor at Karolinska Institutet and senior consultant in geriatric medicine at Karolinska University Hospital, said in a press release.²

Published in the European Heart Journal, the analysis included 7308 patients with concomitant AF and Alzheimer disease identified through SveDem, the Swedish Register for Cognitive Disorders/Dementia. Investigators created 3 matched groups comprising patients treated with NOACs, those treated with warfarin, and those receiving no oral anticoagulant. Cognitive function was monitored longitudinally with the standardized Mini-Mental State Examination (MMSE).¹

Patients receiving NOACs had a significantly slower rate of cognitive decline than those receiving warfarin or no anticoagulant. The estimated difference was slightly more than 0.2 MMSE points annually. However, the source report did not provide group-specific MMSE trajectories, confidence intervals, or the duration over which the difference was assessed.¹,²

“The difference is modest for an individual patient from one year to the next, but over a longer period even such an effect could influence how cognitive function develops,” Nanbo Zhu, a researcher at Karolinska Institutet, said in the press release. “Our findings suggest that NOAC treatment may also be significant for cognition in this patient group.”²

AF is common among older adults, including patients with Alzheimer disease, and anticoagulants are used to reduce thromboembolic risk. NOACs and warfarin interfere with blood coagulation through different mechanisms, but the study report did not identify individual NOAC agents or present drug-specific analyses. Previous research has examined whether anticoagulation is associated with a reduced likelihood of developing dementia; its relationship with progression after Alzheimer disease is established remains less clear.²

Beyond cognition, NOAC treatment was associated with lower risks of death, stroke, thromboembolism, and fractures compared with no anticoagulation. Warfarin was also associated with lower risks of death, stroke, and thromboembolism than no treatment, but it was associated with a higher risk of major bleeding. Numerical effect estimates for these outcomes were not included in the source summary.¹,²

The findings support a potential cognitive advantage for NOACs but do not establish that anticoagulation directly slows Alzheimer disease progression. Treatment selection may reflect comorbidity, frailty, bleeding risk, access to care, or clinician judgment, creating residual confounding despite matching. The investigators also noted that medication switching during follow-up could have affected exposure classification.¹

Consequently, the approximately 0.2-point annual MMSE difference should not be interpreted as evidence for prescribing NOACs specifically to treat cognitive decline. Anticoagulant decisions still require individualized assessment of thromboembolic and bleeding risks. Randomized evidence or additional analyses with detailed exposure, adherence, bleeding, and cognitive data would be needed to determine whether the observed association is causal and clinically durable.

Study funding included support from the Swedish Research Council, Swedish Brain Foundation, CIMED, ALF project funding, and Karolinska Institutet. Eriksdotter reported consulting or speaking relationships involving several pharmaceutical companies; no other conflicts were reported.²

References

1. Zhu N, Xu H, Garcia-Ptacek S, Mitra S, Eriksdotter M. Oral anticoagulants, cognition, and clinical outcomes in atrial fibrillation and Alzheimer’s disease: a Swedish nationwide study. Eur Heart J. Published online August 12, 2026. doi:10.1093/eurheartj/ehag584
2. Karolinska Institutet. People with both atrial fibrillation and Alzheimer’s disease who are treated with modern NOAC blood-thinning medicines may experience a slower rate of cognitive decline. Published August 12, 2026. Accessed August 13, 2026. https://news.ki.se/blood-thinning-medication-linked-to-slower-cognitive-decline