Aspirin was tied to a steep drop in dementia in one narrow slice of a large trial: among older adults in the highest 20% of platelet-count polygenic scores, 1% of those taking low-dose aspirin developed dementia, against 3.3% of those given placebo. In the same group, major bleeding struck 4.4% of aspirin users and 2.1% of placebo recipients, a little more than double the rate. The analysis used genetic data from more than 13,500 volunteers and came from researchers at Monash University, who describe it as a lead to test rather than a result that changes what anyone should do.
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The subgroup matters because the whole trial found nothing. Dr. Peter Fransquet, a research fellow in Monash’s School of Public Health and Preventive Medicine and the lead author, said previous trials found aspirin didn’t prevent dementia when everyone was considered together. His team went back into the ASPREE trial (Aspirin in Reducing Events in the Elderly), which gave healthy older adults a daily low-dose tablet or a placebo, to ask whether inherited biology decided who gained and who only bled. In one corner of the data, the answer appeared to be yes, with a serious catch attached.
The Platelet-Count Polygenic Score Behind the Subgroup
The work appeared in Alzheimer’s & Dementia, the journal of the Alzheimer’s Association, published as “Platelet count polygenic scores may modify the effect of aspirin in primary prevention of dementia”. The wording carries its own hedge: “may.” Monash announced the result in a university release dated Sept. 29, 2026, and ScienceDaily reposted it on Oct. 25, weeks later. According to the Medical Republic’s report on the paper, the analysis covered 13,541 ASPREE participants with a mean age of 75, 54.8% of them women, followed for a median of 4.6 years, during which 345 developed dementia.
A polygenic score folds thousands of small genetic differences into one ranking. Here the scores tracked genetic influences on platelet count, and participants were sorted from lowest to highest. The Medical Republic described a wide search: 5,182 scores were screened, 1,848 survived quality control, 112 showed a nominally significant interaction with aspirin, and only three highly correlated platelet-count scores stayed significant after correction for multiple testing. The top fifth of the leading score became the subgroup. Because the trial was not designed to test aspirin in people with this profile, the finding is a post hoc subgroup result, not a general one.
Dementia and Bleeding Rates in the Top Fifth
Within that top fifth, the hazard ratio for dementia on aspirin versus placebo was 0.28 (95% confidence interval 0.15 to 0.52), the Medical Republic reported, which Monash rounds to a relative risk about 70% lower. In plain rates that is 1% versus 3.3%, a gap of 2.3 percentage points, or about five fewer dementia cases per 1,000 person-years. Placebo recipients in this group had more dementia than the cohort as a whole, a detail that makes the contrast look larger.
Bleeding moved the other way. The hazard ratio for major bleeding on aspirin was 2.13 (95% confidence interval 1.36 to 3.34), with 4.4% of aspirin users and 2.1% of placebo users affected, an absolute increase of 2.3 percentage points, or about five extra major bleeding events per 1,000 person-years. The two gaps are almost mirror images: roughly as many dementia cases avoided as serious bleeds added. All-cause mortality did not differ between aspirin and placebo in this group, according to the same report.
The ASPREE design itself is described in the Medical Republic’s report as a test of 100 mg of aspirin a day in healthy older adults aged at least 70 in Australia and the United States, or 65 for U.S. minority participants, with no prior cardiovascular disease, dementia or physical disability. Those entry rules shape who the result could ever apply to.
The authors and outside experts call the mechanism unproven
Dr. Thomas Holland, a physician scientist at Rush University who was not part of the study, told Newsweek that platelet biology’s role in dementia risk is “only a proposed mechanism rather than a proven explanation,” and that aspirin is “by no means a benign medication.” Fransquet agreed the result needs to be independently confirmed and is not sufficient to change recommendations regarding aspirin use, according to the same Newsweek account.
The signal has other limits. It appeared only at the extreme upper end of the score distribution, a continuous platelet score was not significantly associated with dementia overall or among placebo recipients, and aspirin showed no significant interaction with the APOE gene or with scores for Alzheimer’s and dementia risk. Fransquet said the signal was not linked to established Alzheimer’s and dementia genetic risk factors, which leaves the biology unexplained. The ScienceDaily and Monash accounts give no follow-up or funding detail, and the subgroup’s size per arm was not reported there.
Fransquet put the practical message plainly: people shouldn’t start taking aspirin to prevent dementia on the basis of this study, given the higher bleeding risk. The stakes explain the interest. Dementia Australia estimates about 446,500 Australians are living with dementia in 2026, with the number projected to pass one million by 2065, and the Medical Republic noted that no medicines are approved for primary prevention. The step the authors name is confirmation in other studies and then a trial built for people with this genetic profile, which could show whether the 70% relative reduction survives a prospective test and whether the doubled bleeding risk persists.
This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.
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