AMONG WOMEN with polycystic ovary syndrome/polyendocrine metabolic ovarian syndrome (PCOS/PMOS), any association with Alzheimer’s disease is likely to be mediated by metabolic comorbidities rather than the condition itself, a new review has indicated.
PCOS/PMOS is a common endocrine disorder with significant metabolic and reproductive implications, and attention has increasingly focused on its potential long-term neurological consequences, including cognitive impairment and Alzheimer’s disease, through overlapping biological pathways. However, direct epidemiological evidence linking PCOS/PMOS to increased dementia incidence has remained limited and inconsistent, and it was unclear how far coexisting metabolic dysfunction accounted for any association.
Researchers conducted a comprehensive PubMed search from inception through October 2025 to identify studies examining cognitive performance, brain structure and function, neurodegenerative biomarkers and dementia risk in patients with PCOS/PMOS. Evidence on the biological pathways connecting PCOS/PMOS to Alzheimer’s disease was also synthesised.
The review identified multiple potential mechanistic pathways, such as insulin resistance, chronic inflammation, hormonal dysregulation and cardiovascular dysfunction, which converged on impaired amyloid-β (Aβ) clearance, oxidative stress and cerebral metabolic deficits. Patients with PCOS/PMOS exhibited mild but reproducible impairments in executive function and memory, alongside hippocampal and white matter changes and altered network connectivity, although these findings were influenced by coexisting metabolic dysfunction.
In a retrospective cohort study of 16,531 patients with PCOS/PMOS and 49,335 age-matched controls, dementia prevalence was higher in patients with PCOS/PMOS (0.48% versus 0.22%), and mean age of onset was younger (43 versus 62 years). However, a prospective UK Biobank analysis of 1,008 women with PCOS/PMOS and 5,017 controls matched for age and body mass index found no significant association with all-cause dementia incidence, even when stratified by androgenic phenotype.
Current evidence has indicated that any association between PCOS/PMOS and Alzheimer’s disease risk is likely mediated by metabolic comorbidities, particularly insulin resistance and obesity, rather than an independent effect of the condition itself. Clinical evidence for cognitive vulnerability and dementia remains inconsistent, and cognitive benefits from PCOS/PMOS-specific interventions are lacking. Clinical focus should therefore remain on optimising metabolic health, while longitudinal and interventional studies are required to clarify long-term neurological relationships and outcomes.
Reference
Amiri M et al. Potential links between PCOS/PMOS and alzheimer disease and related dementias. Journal of the Endocrine Society. 2026;10(11):bvag206.
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