Review evidence on associations between polyendocrine metabolic ovarian syndrome (PMOS/PCOS) and cognitive function, brain changes, Alzheimer’s disease (AD) biomarkers, and dementia.
Approach:
Search: Investigators searched PubMed from inception through October 2025, without language or study-design restrictions.
Evidence reviewed: The review included observational, case-control, neuroimaging, biomarker, and preliminary intervention studies, assessing cognition, brain structure and function, biomarkers, dementia incidence, and metabolic or endocrine factors.
Key Findings:
Dementia evidence was inconsistent: one retrospective cohort found higher dementia prevalence and earlier onset among patients with PMOS, while a UK Biobank analysis found no significant association with incident dementia, including by androgen phenotype.
Studies reported mild differences in executive function, attention, and memory; some were more closely associated with insulin resistance and glycemic control than with PMOS status or androgen levels.
Neuroimaging studies reported hippocampal, white matter, connectivity, and glucose-metabolism differences. In a small study, cerebral glucose metabolism was 9%–14% lower in patients with PMOS and inversely correlated with insulin resistance.
AD-related biomarker findings varied and appeared less pronounced in metabolically healthy patients; most studies measured peripheral rather than brain biomarkers.
Preliminary treatment studies reported inconsistent changes in selected cognitive measures or brain activation.
Interpretation:
The authors stated that any association between PMOS and AD is likely mediated by metabolic comorbidities rather than an independent PMOS effect. They noted that evidence for independent hormonal contributions remains limited.
Limitations:
Studies varied substantially in design, and many cognitive and neuroimaging studies had small samples.
Adjustment for metabolic confounders was inconsistent, and longitudinal evidence was limited.
Most biomarker studies used peripheral measurements rather than direct evidence of AD-related brain pathology.
Conflicting dementia findings and preliminary intervention evidence do not establish long-term risk or whether treatment changes cognitive decline or dementia incidence.
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