Recent research indicates that ovaries may have a significant impact on postmenopausal health, contradicting the belief that they become completely inactive after menopause. Studies show that immune cells infiltrate the ovaries of aging mice, linking these organs to chronic postmenopausal inflammation.

“We assumed the ovaries fulfilled their purpose after reproduction,” stated Francesca Duncan from Northwestern University. “Our findings were quite unexpected.”

In March, Duncan and her team published a study that explored the protein profiles of postmenopausal women aged 50 to 75. Contrary to their expectations of uniformity, they discovered that the molecular signatures of the ovaries evolve dramatically over time, challenging the notion of their inactivity.

To delve deeper, Duncan’s team is analyzing mouse ovaries, focusing on tissue and gene expression at different life stages: young (2 months), reproductive (18 months), and post-reproductive (24 months). Despite lacking menstrual cycles, aging mice experience a decline in egg reserves leading to irregular cycles, similar to human menopause. “We recognize that the hormonal changes mirror what happens in humans as they age,” Duncan noted.

Initial findings confirmed some expectations; older ovaries exhibited a loss of egg-producing follicles and increased scarring. However, the study also found heightened gene activity associated with inflammation and immune response as aging progressed. The number of immune cells, including T cells and macrophages, rose in tandem with age.

Further investigation is crucial to clarify the implications of these changes for immunity and overall health. Duncan suggests this transformation in the ovaries might indicate a loss of reproductive function coupled with an increase in immune activity, which may not be beneficial. “As ovaries transition, there could be an uptick in inflammatory signaling that interacts with other bodily systems,” she explained.

While the current study focuses on mice, Diana Laird and her team at UCSF propose that similar immune modifications may be occurring in human ovaries, based on shared reproductive traits across species. “Both our species cease cyclical activity once the ovarian supply is depleted. Other phenomena, like fibrosis and altered nerve supply, are also present,” she asserted.

Although the rationale behind this evolutionary change in older mice remains unclear, it may have historically provided a survival advantage by enabling immune cell reservoirs at a time when fewer individuals lived to old age. Today, however, it poses risks of inflammation and autoimmune disorders.

This research prompts a reevaluation of the ovaries’ importance post-menopause. Although typically seen as dormant, they continue to release hormones like androgens, crucial for maintaining bone density and libido. Laird emphasized the need for more in-depth studies, linking immune changes in the ovaries to increased inflammation and conditions like rheumatoid arthritis after menopause. “This emphasizes the necessity for detailed investigations into the post-reproductive ovary’s cellular and molecular components,” she concluded.