Scientists at Northwestern University in Illinois have discovered that ovaries after menopause may not simply become dormant, as previously assumed, but could instead undergo a fundamental identity shift that links them to inflammation in the body. The research, led by reproductive biologist Francesca Duncan, examined the ovaries of mice at different reproductive stages and found that as the animals aged, their ovaries became increasingly infiltrated with immune cells such as T cells and macrophages.
The study, which has not yet been peer-reviewed, analysed tissue and gene expression in young (2 months), reproductively old (18 months) and post-reproductive (24 months) mice. While the older ovaries predictably lost egg-producing follicles and showed more scarring, the team also observed a marked upregulation of genes associated with inflammation and immune activity. Duncan described the finding as 'super surprising', noting that the organ appears to be 'losing the reproductive signature and taking on an immune signature'.
Duncan suspects this change may contribute to 'inflammaging' — the chronic, low-grade inflammation that accompanies ageing. She suggested that post-reproductive ovaries could release inflammatory signalling molecules that communicate with other parts of the body. 'It is possible this post-reproductive change means nothing, but it's also possible it's sending out these signals,' she said. The researchers point out that mice do not undergo human-style menopause but do experience age-related decline in fertility and hormonal function, making them a valid model.
Diana Laird, a reproductive biologist at the University of California, San Francisco, who was not involved in the study, said similar immune changes likely occur in humans given the reproductive similarities between the species. Both organisms stop cycling when their supply of immature egg cells falls below a critical threshold, and both share changes such as fibrosis and increased nerve distribution. Laird noted that the findings add to growing evidence that immune alterations in the ovaries may be behind the increased inflammation that drives conditions like rheumatoid arthritis after menopause.
The implications for UK healthcare could be significant. Currently, healthy ovaries are generally left in place after menopause because they continue to produce androgens, which help maintain bone density and libido. However, if post-menopausal ovaries are found to contribute to systemic inflammation, this could reshape medical advice around ovarian retention and removal. Duncan stressed that further research is needed, and the study was limited to mice, but she called the results a 'call to action' for more work on the post-reproductive ovary.