Researchers examined clinical records and genomic data for 187,341 adults aged 50 and older drawn from the NIH All of Us Research Program, the source reported. Within that cohort, 3,026 participants had a clinical diagnosis of ADHD. The investigators observed that 6.7% of participants with ADHD went on to develop mild cognitive impairment, compared with 3.4% of those without ADHD. Those raw proportions translated, in the authors’ analysis, into a more-than-fourfold increased risk of cognitive impairment among people with clinically defined ADHD. The association remained after statistical adjustment for age, biological sex, and comorbidities, the study team reported.
The authors also calculated a genetic risk score for ADHD. When participants were grouped by that genetic liability, people with the highest genetic risk had 35% greater odds of developing dementia than those with the lowest genetic risk, investigators reported. The study appears in JAMA Psychiatry and was led by researchers at the University of Pittsburgh School of Medicine; Douglas Teixeira Leffa, MD, PhD, served as a co–first author and described the work to Medical News Today.
The current dataset did not include a causal analysis of biological pathways, and the study did not test mechanisms linking ADHD to later cognitive decline, the source stated. The article noted prior work from other groups that may offer hypotheses but did not supply complete imaging or mechanistic results in the report reviewed. In interview comments, Dr. Teixeira Leffa framed the study’s contribution as providing two complementary lines of evidence — clinical diagnosis and genetic liability — that both point toward an association between ADHD and later-life cognitive problems. He said that this dual approach reduces the likelihood that the observed relationship is purely an artifact of how ADHD is recorded in health records, according to the source.
The investigators used electronic health records linked to genomic data from the All of Us Research Program, a large NIH cohort, the article reported. The analytic sample included adults aged 50 and older; the article provided the total sample size and the count of participants with clinical ADHD, but did not report additional demographic breakdowns, detailed comorbidity prevalence, or follow-up duration in the sections cited. The team adjusted their primary comparisons for chronological age, sex, and comorbid conditions; the association between clinical ADHD and cognitive impairment persisted after those adjustments, according to the source.
The source also reported the authors’ use of a genetic risk score to estimate ADHD liability. The piece did not specify the genetic variants used, the precise construction method for the score, or the thresholds applied to define “highest” versus “lowest” genetic risk; those methodological details were not provided in the source article.
The source article highlighted several concrete gaps that remained after this analysis. The study did not probe mechanisms linking ADHD to mild cognitive impairment or dementia; causality therefore cannot be inferred from these associations alone. The article also did not report complete imaging, biomarker, or longitudinal mechanistic data in support of a biological pathway, and it did not include the detailed methodological description of the genetic-risk-score derivation in the sections cited.
Investigators told Medical News Today that longer-term studies will be necessary to clarify whether and how ADHD contributes to later cognitive decline, and to separate the effects of diagnosis, treatment history, lifestyle, and comorbid conditions. The source noted that previous imaging studies exist but did not provide their full findings in this report. Those unanswered questions — about timing, mechanism, and potential modifiable contributors — represent the next steps the authors said are needed before clinical recommendations could change based on these associations.
The article and its underlying paper in JAMA Psychiatry provide population-level evidence of an association between clinical and genetic markers of ADHD and later cognitive impairment. They do not, however, establish mechanism or causation. The source concluded by calling for further longitudinal and mechanistic work to determine whether ADHD itself raises dementia risk or whether shared risk factors account for the observed relationships.