Key Takeaways
Ovaries do not go dormant after menopause; they appear to take on a new, immune-related role.
The core finding comes from mice, but it fits a pattern already documented in earlier human studies.
The shift may help explain why aging affects the body differently after menopause.
Confirmation in humans is still developing; this is early-stage science.
For decades, scientists believed the ovaries became largely inactive after menopause. Egg production stops, and estrogen and progesterone levels decline sharply, leading many researchers to view the ovaries as an organ that had largely completed its role. However, a 2026 study published in Molecular Human Reproduction suggests the postmenopausal ovary remains biologically active by shifting toward immune activity rather than simply becoming dormant.1
Women go through the post-menopausal period of life for more than a third of their existence, while surprisingly little has been known about what the ovary does during that time. Scientists from the Northwestern University's Feinberg School of Medicine started studying the changes that happen in the ovaries throughout the aging process using mice as a model organism.
Although this study was conducted in mice, earlier human studies have also documented inflammatory and immune-related changes in aging ovaries, suggesting this area of research may have relevance beyond animal models.²
The research suggested that rather than shutting down, the post-reproductive ovary appears to shift its identity, taking on functions associated with the immune system (behaving more like immune tissue).1
In order to investigate the changes that occur in the course of this process, mice were examined at different life stages: young and fertile (2 months), aging and still fertile (18 months), and post-fertile (24 months, beyond the stage known as oopause among mice biologists).1 The term "oopause" refers to the cessation of the ability of mice to produce eggs (ovulation), similar to menopause in women; however, the mice do not menstruate or experience in hormonal decline.1
One ovary of each individual mouse was examined using a microscope for its physical structure, while the paired ovary was tested for gene activity.1 This paired design let researchers see not just what the tissue looked like with age, but what the cells were doing at a molecular level.
The onset and duration of the postreproductive period differ between mice and humans, and it remains unclear whether older ovaries in humans behave identically. The mouse model is useful for mapping biological mechanisms, not for predicting an exact human timeline.
Speaking to Science, senior author Francesca Duncan of Northwestern University's Feinberg School of Medicine said:
I was super excited to be part of the initiative, but I was also bummed to be looking at ovaries that were essentially non-functional. For me, that was really eye-opening because if this organ is not doing anything, you would predict that there would be no changes across age. It would all look the same. This highlighted to us that there’s something else going on with this organ.Francesca Duncan, Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA told Science.
By the post-fertile stage, the mice had run out of ovarian follicles (fluid filled sac housing an immature egg) entirely, and their ovaries had grown noticeably stiffer due to a buildup of collagen (glue like substance that holds tissue together).1
Genes responsible for ovarian function and production of reproductive hormones were turned off, as expected. But surprisingly, inflammatory, immune system, and white blood cell communication genes were turned on. Upon examining these aged ovaries under a microscope, researchers found that the aged ovaries contained T cells, macrophages, and giant cells which is characteristic of immune tissue, not reproductive tissue.1
The scientists noted that based on the analysis of aged ovaries, they had expected the production of signaling molecules, which could get into the bloodstream, meaning that the ovaries could send messages to other parts of the body.1 But this hasn't been confirmed yet for human tissues. Researchers caution that it is still uncertain whether older ovaries participate in immune signaling or they just become a site for immune cell accumulation.
The bloodstream signaling angle is where the study's implications helps explain ovarian function after menopause. The study's senior researcher has explained to Science that the post-reproductive ovary could secrete molecules (immunoglobulin/ complement proteins) that predispose the body to chronic, low-level inflammation during the menopausal years.
That idea, if confirmed, could speak to a long-standing puzzle in aging research: women tend to experience more chronic illness in later life despite living longer than men on average. An ovary that continues producing inflammatory signals for years after menopause offers one possible, though still speculative, piece of that puzzle.
The 2026 mouse study did not emerge in isolation. Earlier research already pointed toward inflammation building up in aging ovarian tissue. Human studies have found that specific inflammatory signaling proteins rise in ovarian fluid starting around age 38, well before menopause itself.2 Separately, researchers using spatial mapping techniques have begun locating aging, senescent cells directly within postmenopausal human ovarian tissue, an area that had previously been difficult to characterize in detail.3
There are also early hints that this inflammatory shift might not be fixed. In mice, giving the diabetes medication metformin after reproductive failure reduced ovarian inflammatory activity and changed the mix of immune cells present.2 A related finding from a 2026 Research Square preprint reported that metformin could reverse an age-related increase in a specific type of immune cell within postmenopausal ovarian tissue. Because this evidence comes from a preprint, it has not yet undergone peer review. 3 These findings are preliminary and do not amount to a treatment recommendation, but they suggest the postmenopausal ovary's new immune identity may not be a fixed, one-way process.
Taken together, researchers reviewing this body of work note that it remains unresolved whether ovarian inflammation is a cause of ovarian aging, a consequence of it, or some combination of both.2,3 That open question is likely to shape the next wave of research into what the ovary does long after its reproductive role has ended.
No. They stop releasing eggs and making most of their hormones, but they don't just switch off. New research shows they stay biologically active in a different way, taking on a role linked to the immune system.
Yes, a little. They stop making most of the estrogen and progesterone they used to, but they still make small amounts of other hormones called androgens. Newer research also suggests they may release other chemical signals tied to inflammation, not just hormones.
No. This study did not examine ovarian cysts, ovarian masses, or cancer risk. Instead, it investigated how aging ovaries may change biologically after menopause. While researchers speculate that immune-related changes in the ovaries could influence healthy aging, this study does not suggest that postmenopausal women are at increased risk of ovarian cysts or masses because of these findings.¹ ²
There are early hints that it might be possible. In mouse studies, a common diabetes medicine called metformin seemed to calm down this inflammation. A small human study found something similar. But this is very early research, not a treatment doctors currently recommend for this purpose.
Converse, Aubrey, Shweta S. Dipali, Ian P. Schowe, Emmett B. Kelly, Shivani S. Jambunathan, Sarah R. Ocañas, Michael B. Stout, Michele T. Pritchard, and Francesca E. Duncan. "The Post-Reproductive Ovary Shifts from a Reproductive to an Immune-like Organ." Molecular Human Reproduction 32, no. 2 (2026): gaag038. https://doi.org/10.1093/molehr/gaag038.
Isola, José V. V., Jessica D. Hense, César A. P. Osório, Subhasri Biswas, José Alberola-Ila, Sarah R. Ocañas, Augusto Schneider, and Michael B. Stout. "Reproductive Ageing: Inflammation, Immune Cells, and Cellular Senescence in the Aging Ovary." Reproduction 168, no. 2 (2024): e230499. https://doi.org/10.1530/REP-23-0499.
Schilling, Birgit, Mark Watson, Pooja Devrukhkar, et al. "Senescence-Linked Fibrosis in the Aging Human Ovary Revealed by p16-Based Histological Profiling and Spatial Transcriptomics." Preprint, Research Square, version 1, posted February 5, 2026. https://doi.org/10.21203/rs.3.rs-8290960/v1.