Stillbirth and risk of Alzheimer’s disease and other related dementias: Findings from the Utah Population Database (1977–2024)
Abstract
Introduction:
Prior studies suggest stillbirth increases dementia risk in women, but findings are inconsistent and largely based on non‑U.S. cohorts with self‑reported reproductive histories and limited assessment of dementia subtypes. Stillbirth is linked to maternal vascular and stress‑related conditions characterized by inflammation and thrombosis, biological pathways that also contribute to neurodegeneration We examined associations of stillbirth with dementia overall and dementia subtypes in a large U.S. population.
Methods:
We conducted a retrospective cohort study using the Utah Population Database. Assigned females at birth aged 15–55 with ≥1 pregnancy (1978–2023) were followed for dementia and death through 2024. Stillbirth was identified from fetal death records and dementia from electronic medical records and death certificates. Cox models estimated hazard ratios (HR) for all-cause dementia and dementia subtypes with 95% confidence intervals (CI). Models used age as the analysis time scale, censoring on out-migration, death, or end of follow-up. Early (<65) vs late‑onset (≥65) dementia were prespecified to reflect clinically and etiologically distinct onset periods. Models adjusted for birth year, baseline parity, and age at index pregnancy.
Results:
The cohort included 910,322 women and 4,916 dementia cases (Table 1). Overall, 11,795 women experienced ≥1 stillbirth (73 dementia cases). Stillbirth history was associated with increased risk of any dementia (HR = 1.32, 95% CI 1.05–1.66), driven by early‑onset dementia (HR = 1.50, 95% CI 1.07–2.11), particularly non‑Alzheimer’s (namely vascular dementia), early‑onset subtype (HR = 1.54, 95% CI 1.05–2.26). No associations were observed for late‑onset dementia or Alzheimer’s disease.
Conclusion:
Stillbirth was linked to elevated dementia risk, particularly early‑onset and non‑Alzheimer’s subtypes. This pattern suggests that reproductive vascular insults may increase neurodegenerative vulnerability.

