Aspirin May Be Linked to 70% Lower Dementia Risk in Certain People, Study Finds
Andrea Powell
A surprising new analysis from Monash University suggests that low-dose aspirin may significantly cut dementia risk for some older adults, but only for those with a particular genetic profile. The findings highlight the emerging promise of personalized dementia prevention and underscore the long standing tension between potential benefits of aspirin and its risk of serious bleeding.
The research, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, dug into genetic data from more than 13,500 participants in the ASPREE Trial (Aspirin in Reducing Events in the Elderly). Earlier results from ASPREE indicated that aspirin did not prevent dementia when everyone in the trial was analyzed together. That outcome aligned with other large studies that failed to show a broad memory protection effect from routine aspirin use in older adults.
This new investigation asked a more targeted question. Instead of looking at the group as a whole, researchers examined inherited differences between participants, using genetic scores to see whether certain people might respond to aspirin differently than others. The focus was on whether any specific pattern in a person’s DNA might help predict who could gain a dementia prevention benefit from low-dose aspirin.
The strongest signal turned out to involve platelets, the tiny blood cells that help form clots. The team created a genetic score associated with platelet count and then sorted participants according to that score. Individuals in the highest 20 percent on this measure became the focal group. Researchers then compared dementia outcomes between people in that group who received aspirin and those who received a placebo.
In this high platelet count genetic group, the difference in dementia diagnoses was striking. Dementia developed in 1 percent of those who took aspirin, compared with 3.3 percent of those given a placebo. Put another way, this translated into about a 70 percent lower relative risk of dementia for aspirin users in that subgroup. The absolute risk reduction, however, was more modest. The difference of 2.3 percentage points equaled roughly 23 fewer dementia cases per 1,000 people.
Lead author Dr. Peter Fransquet, a research fellow at Monash’s School of Public Health and Preventive Medicine, suggested that these results move the field closer to a more personalized approach to dementia prevention. He noted that earlier trials concluded aspirin did not prevent dementia when all individuals were grouped together. This study indicates that, for a genetically defined subset, the story may be different. It raises the possibility that inherited traits related to platelet biology might one day guide decisions about preventive treatments such as low-dose aspirin.
The other side of the equation is crucial. The same genetic group that appeared to gain dementia protection also experienced a higher rate of serious bleeding. In those with high platelet count genetic scores, major bleeding occurred in 4.4 percent of aspirin recipients and 2.1 percent of placebo recipients. That is an excess of about 23 additional major bleeding events per 1,000 people, mirroring the size of the dementia benefit in the opposite direction.
This balance between lower dementia risk and increased bleeding risk lies at the heart of the study’s implications. Aspirin has long been known to raise the chance of serious bleeding, especially in older adults. Its blood thinning effect, beneficial for preventing clots, also makes dangerous bleeding in the brain or gut more likely. The ASPREE Trial itself was designed to look carefully at risks and benefits of aspirin in healthy older people, and bleeding has always been a central concern.
What I found especially striking is the biological clue that emerges from this analysis. The genetic signal that predicted who might benefit from aspirin was not linked to the well-known genetic risk factors for Alzheimer’s disease and dementia. Instead, it pointed directly toward platelet count. Scientists have previously connected platelet activation and aggregation, or clumping, with dementia, but the role of overall platelet numbers remains less clear. This study strengthens the idea that platelets are more than just clotting agents. They may play an underappreciated part in the processes that damage the brain over time.
Dr. Fransquet emphasized how this platelet linked genetic pattern provides a new avenue for understanding dementia. It suggests that brain health in later life may be influenced by fine-grained aspects of blood biology, not only by familiar genes that affect amyloid or tau proteins in Alzheimer’s disease. For researchers, this could open fresh paths for studying how vascular and clotting pathways intersect with cognitive decline.
For individuals and clinicians, however, the message is not to rush toward aspirin as a dementia prevention strategy. The study is exploratory and identifies a group worth deeper investigation rather than offering a ready made prescription. A trial specifically designed around this platelet count genetic profile will be needed to confirm whether the dementia benefit is real and reproducible, and to better understand how that benefit stacks up against the increased risk of serious bleeding.
Dementia Australia estimates that 446,500 Australians will be living with dementia in 2026, with projections suggesting the number could exceed one million by 2065. Against that backdrop, even a modestly effective and affordable preventive treatment for certain people could be enormously important. Aspirin is already cheap and widely available, which makes the possibility of personalized dementia prevention especially compelling if the findings hold up.
At the same time, the bleeding risk remains significant. The results highlight the reality that preventive medicine often involves trade offs, particularly in older adults. The prospect of 23 fewer dementia cases per 1,000 people sits alongside 23 additional major bleeding events in that same group. Any real world strategy would require careful, individualized decision making, taking into account a person’s overall health profile, preferences, and values, ideally informed by genetic testing and robust evidence from dedicated trials.
For now, experts advise against starting aspirin solely to prevent dementia based on this analysis. The authors themselves stress that people should not make changes to their medication without talking to a doctor, particularly given the possibility of serious bleeding. Rather than a call to immediate action, this study serves as a vivid example of how genetic research can reshape the conversation about prevention. It hints at a future where treatments are not judged only in broad averages, but tailored to those whose biology makes them most likely to benefit and least likely to be harmed.