- About 32 million people globally live with Alzheimer’s disease.
- People who have Alzheimer’s disease are at increased risk for several health issues, including atrial fibrillation (AFib).
- Past studies show that anticoagulant medications may help lower a person’s risk of developing dementia.
- A new study says treatment with newer blood-thinning medications, or new oral anticoagulants (NOAC), may help slow the cognitive decline rate of people with both Alzheimer’s disease and AFib.
AFib is a heart rhythm disorder commonly treated with an anticoagulant, or blood-thinning medication. Past studies show that anticoagulants may help lower a person’s risk of developing dementia.
For this study, researchers analyzed medical data for more than 7,300 participants from the SveDem (Swedish Register for Cognitive Disorders/Dementia) database. Selected study participants had both AFib and Alzheimer’s disease.
Participants were broken down into three groups: those treated with NOAC, those treated with the anticoagulant warfarin, and those not treated with an anticoagulant at all.
“Studies have found that about 15–20% of people with Alzheimer’s disease also have atrial fibrillation,” Maria Eriksdotter, MD, PhD, professor in the Department of Neurobiology, Geriatrics, Health Sciences, and Society at the Karolinska Institutet, senior consultant in geriatric medicine at Karolinska University Hospital, and lead author of this study, told Medical News Today.
“Blood thinning medications are widely used to prevent strokes and blood clots. By improving blood flow and reducing small-scale damage to the brain, blood-thinning medications could potentially help preserve cognitive function,” Eriksdotter explained.
“We therefore wanted to investigate whether people with both atrial fibrillation and Alzheimer’s disease who were treated with blood thinning medications experienced a different rate of cognitive decline compared with those who were not on blood thinning medications. In addition, we also compared the modern blood thinning drugs NOAC with the older drug warfarin.”
– Maria Eriksdotter, MD, PhD
At the study’s conclusion, researchers reported that participants treated with NOAC had a significantly slower cognitive function decline rate than those receiving warfarin or no anticoagulant drug.
“This finding suggests that NOAC may offer benefits beyond their established role in preventing stroke and blood clots in people with atrial fibrillation,” Eriksdotter said.
“While the effect was modest, even small delays in cognitive deterioration over several years can be meaningful for patients and families. It also strengthens the indication to treat people with atrial fibrillation and Alzheimer’s disease with NOAC,” she told us.
As for how NOAC may help potentially slow cognitive decline in people with Alzheimer’s disease and AFib, Eriksdotter said at present, they can only speculate about the mechanisms.
“One leading hypothesis is that NOAC may help protect the brain by improving blood flow and reducing small-scale vascular damage,” she detailed. “Another possibility is that NOAC may provide more consistent protection against small blood clots and cerebrovascular events than older treatments.”
“Since vascular disease and Alzheimer’s disease often coexist and can interact, better protection of the brain’s blood vessels could potentially help preserve cognitive function,” Eriksdotter added. “However, our study shows an association, not causation, and more research is needed to understand the biological processes involved.”
MNT had the opportunity to speak with Craig Basman, MD, FACC, FSCAI, associate director of the Structural and Congenital Heart Program, and director of the Structural and Congenital Fellowship Program at Hackensack Meridian Hackensack University Medical Center in New Jersey, who was not involved in this study.
Basman commented that finding NOAC — which are already the standard of care for stroke prevention in AFib — may offer a secondary, neuroprotective benefit in patients who already have Alzheimer’s is ”highly encouraging.”
“It underscores the vital role that optimal cardiovascular management plays in holistic patient health. However, my biggest concern with this study is that this implies association and does not establish causation,” he cautioned.
Given that this was a retrospective observational study, Basman said, the fundamental next step must be prospective, randomized controlled trials to definitively establish causation rather than correlation.
“I would also like to see future studies incorporate advanced neuroimaging, such as longitudinal brain MRIs, to identify the exact mechanisms at play, specifically, verifying if NOAC measurably reduce the burden of cerebral microinfarcts or improve cerebral blood flow,” he added.
“Finally, analyzing the comparative efficacy of specific NOAC agents (e.g., apixaban versus rivaroxaban) will be highly relevant for cardiologists looking to tailor anti-coagulation strategies for this highly vulnerable patient population,” noted Basman.
MNT also spoke with Dung Trinh, MD, an internist for MemorialCare Medical Group and chief medical officer of Healthy Brain Clinic in Irvine, CA, who said that even a modest slowing of cognitive decline can be meaningful for people with Alzheimer’s disease and their families.
“Cognitive decline affects far more than performance on a test,” Trinh, who was likewise not involved in this study, explained.
“It can affect independence, communication, relationships, and a person’s ability to manage everyday activities. There remains a tremendous need for treatments that can preserve cognitive and functional abilities for as long as possible,” he stressed.
“Approaches that may provide benefits while also treating other medical conditions are particularly interesting,” Trinh continued.
“In this study, the difference associated with NOAC use was relatively small, about 0.2 points per year on the Mini-Mental State Examination (MMSE), but even incremental differences may become meaningful over time and warrant further investigation, particularly if they can be achieved while also reducing the risk of stroke,” he noted.
Trinh also emphasized, however, that while these findings are encouraging, they need to be interpreted with caution.
“This was an observational study, so we cannot conclude that NOAC themselves caused the slower cognitive decline,” he explained. “I would not recommend changing anticoagulant therapy solely because of a potential cognitive benefit based on these findings.“
“Rather, the study adds to a growing body of research exploring the important relationship between cardiovascular health, cerebrovascular disease, and Alzheimer’s disease,” he concluded.
