Aspirin is about as ordinary as medicine gets, which is part of why a new dementia finding is turning heads. The idea that such a familiar pill might help prevent dementia is intriguing. What makes this finding especially interesting is that the apparent benefit appeared in only a specific group of people.
A genetic analysis of a major trial in older adults found that people on daily low-dose aspirin had far fewer dementia diagnoses than people on placebo, but only in one narrowly defined slice of the group.
It is easy to see why the headline traveled: a cheap, familiar pill, a dreaded disease, and a number that sounds almost too good to be true. Yet the potential benefit comes with a serious drawback that makes the finding far less straightforward.
Published September 24 in Alzheimer’s & Dementia, the Alzheimer’s Association’s journal, the study raises an intriguing possibility without settling the question. The numbers deserve a closer look, particularly because the analysis was never designed to prove aspirin protects the brain.
Only One Group Saw the Big Drop
This number comes from a small, specific slice of the study.
Researchers analyzed genetic data from 13,541 people enrolled in ASPREE (Aspirin in Reducing Events in the Elderly).
The participants were healthy older adults without prior cardiovascular disease, dementia, or physical disability, and their average age was 75. They received either 100 mg of aspirin daily or a placebo. Over a median of 4.6 years, 345 developed dementia.
The researchers then examined genetic scores to see whether participants responded to aspirin differently. The strongest finding appeared among the top 20 percent of people with a score based on genes associated with platelet count.
In this group, 1.0 percent of aspirin takers developed dementia, compared with 3.3 percent of those taking placebo. That translates to roughly 70 percent lower relative risk, an eye-catching figure by any measure.
But relative risk tells only part of the story. As the published study shows, the absolute difference was 2.3 percentage points, equivalent to about 23 fewer dementia cases per 1,000 people.
And those weren’t the only numbers worth examining.
The Bleeding Numbers Tell the Other Half
Same group, same pill, and a cost that lines up almost exactly.
Among participants with high genetic scores, major bleeding occurred in 4.4 percent of aspirin takers, compared with 2.1 percent of those on placebo. That works out to roughly 23 additional serious bleeds per 1,000 people, matching the dementia difference in size but in the opposite direction.
Over time, the researchers estimated about five fewer dementia cases and five additional major bleeds per 1,000 person-years.
These weren’t minor bleeding incidents. ASPREE defined major bleeding to include hemorrhagic stroke, symptomatic bleeding inside the skull, and bleeding elsewhere serious enough to require hospitalization, transfusion, surgery, or result in death.
Across the full trial, aspirin increased major hemorrhage from 6.2 to 8.6 events per 1,000 person-years, including more upper digestive tract and intracranial bleeding.
The findings are particularly notable because participants had been screened to exclude those at high bleeding risk, including people with anemia or taking blood thinners. Even in this selected population, the risk remained. Deaths from any cause did not differ between aspirin and placebo recipients in the highest-scoring group.
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Your Platelet Count Won’t Give You the Answer
Anyone hoping a routine blood test could point the way will be disappointed.
The genetic score used in the analysis isn’t the same as a platelet count measured during a routine blood test. A polygenic score combines the effects of numerous genetic variants associated with platelet count, rather than simply measuring how many platelets are present.
That distinction matters. The study establishes no clinical cutoff, so a person with a high platelet count cannot assume aspirin would reduce their dementia risk.
Previous work has linked platelet activation and clumping with dementia, although the significance of overall platelet count remains less certain.
Interestingly, the researchers found no significant interaction between aspirin and APOE genotype, or with genetic scores associated with Alzheimer’s disease and dementia risk. Instead, the findings pointed to platelet biology.
There was another curious result. Placebo recipients in the highest-scoring group developed dementia more frequently than the broader study population, raising the possibility that extremely high genetically predicted platelet counts carry their own dementia risk.
However, the continuous genetic score showed no significant association with dementia across the full cohort or among placebo recipients. If such a connection exists, it may be limited to the extreme upper end of the genetic distribution.
Why Researchers Went Digging at All
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Aspirin already had its shot at the broad prize and came up empty.
The original ASPREE trial included 19,114 participants, with 9,525 assigned to aspirin and 9,589 to placebo. After a median follow-up of 4.7 years, low-dose aspirin did not significantly reduce cardiovascular disease or improve the trial’s main outcome of survival without disability.
The dementia results were similarly disappointing. As Fransquet explained in a Monash University release: “Previous trials found aspirin didn’t prevent dementia when everyone was considered together.”
That broader failure prompted researchers to examine whether genetics might explain why some participants responded differently.
They screened thousands of polygenic scores, with more than 1,800 passing quality checks. After correcting statistically for the large number of comparisons, only three closely related platelet scores remained significant.
Crucially, this genetic investigation took place after the original trial ended. It was an exploratory analysis, not a trial specifically designed to establish whether aspirin could prevent dementia in people carrying these genetic characteristics.
That leaves an interesting finding, but not yet a confirmed preventive strategy.
What Has to Happen Next
The researchers have a short list of things they need to see first.
Before the findings can influence clinical decisions, researchers need to establish whether the same relationship appears in other populations. Ultimately, that means running a trial focused specifically on people with the relevant genetic profile.
The interest is understandable. No medication is currently approved specifically for primary prevention of dementia, while Dementia Australia estimates that 446,500 Australians are living with the condition in 2026. That number is projected to exceed 1 million by 2065.
Still, the biological explanation for aspirin’s apparent effect in this group remains uncertain. Nor does the study provide a validated way to turn someone’s genetic profile into a practical testing and treatment plan.
For now, that leaves a question beyond whether aspirin might help: if a genetic test could someday identify both a possible benefit for your memory and a serious risk, how much certainty would you want before taking that pill?
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