
A comprehensive review of earlier research studies suggests polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is linked to brain changes associated with Alzheimer’s disease and dementia such as memory loss.
“Clinically, PMOS patients exhibit mild but reproducible impairments in executive function and memory, alongside structural and functional brain alterations, which could suggest greater risk for Alzheimer’s disease and dementia,” said lead study author Ricardo Azziz, MD, of the University of Alabama at Birmingham, in a press statement.
“Current evidence suggests that any association between PMOS and Alzheimer’s disease and dementia is likely mediated by metabolic comorbidities, particularly insulin resistance and obesity, rather than an independent effect of PMOS itself.”
PMOS is estimated to affect roughly 6–11% of women of reproductive age around the world, although estimates differ depending on how the condition is diagnosed. It is characterized by excess activity of male sex hormones such as testosterone, irregular or absent periods, and sometimes cysts on the ovaries. Many women with this condition also have metabolic complications like insulin resistance, higher body weight, and persistent low-grade inflammation.
Azziz and co-authors of the review, published in the Journal of the Endocrine Society, searched PubMed for studies examining whether PMOS is linked to cognitive changes, brain imaging findings, Alzheimer’s-related blood biomarkers, or dementia. They also reviewed possible shared biological mechanisms, including insulin resistance, obesity, inflammation, hormonal disturbance, and cardiovascular risk.
The team included 21 studies published between 2007 and 2025 including at least 75,000 participants across the different studies. The results showed women with PMOS showed mild, inconsistent differences in attention, executive function and memory. Some imaging studies reported brain changes such as altered white-matter structure, hippocampal or amygdala-volume differences, altered functional connectivity, and lower brain glucose metabolism. A few studies also found Alzheimer’s-related proteins in blood.
The signals of Alzheimer’s or dementia appeared to track most strongly with metabolic ill health such as insulin resistance, obesity, poor glucose control, and cardiovascular risk rather than with PMOS itself. Findings were weaker or absent in metabolically healthy, non-obese, insulin-sensitive women with PMOS.
PMOS patients are not currently eligible for routine cognitive screening or dementia risk counseling, despite the research pointing to these people being at higher risk than the general population.
“Despite growing knowledge, critical gaps persist … It remains unknown whether PMOS independently increases Alzheimer’s disease risk or whether observed associations are mediated through insulin resistance, inflammation, and vascular dysfunction,” write the authors.
“Large-scale, prospective cohort studies spanning the reproductive lifespan are urgently needed… Substantial gaps exist in understanding shared molecular mechanisms. Genetic overlap between PMOS and Alzheimer’s disease remains undefined, and the roles of miRNA–mRNA networks, epigenetic modifications, and metabolic signaling pathways require direct investigation. Finally, whether PMOS management can meaningfully alter long-term cognitive trajectories remains unanswered,” they conclude.


