Scientists identify protein linked to female fertility decline

Researchers presented at the Fertility 2026 conference in Edinburgh, Scotland, evidence that the reduction of a specific protein contributes to egg deterioration with age in women. The study, not yet peer-reviewed, suggests restoring this protein could improve egg quality in in vitro fertilizations. Experts view the work as a promising step, though it won't resolve all infertility cases.

Scientists are advancing in understanding the decline in female fertility with age, a central mystery in human reproduction. Presented at the Fertility 2026 conference in Edinburgh, the study led by Melina Schuh from the Max Planck Institute and Agata Zielinska, co-founder of Ovo Labs, identified the drop in Shugoshin protein levels as a key factor. This protein, whose Japanese name means 'guardian spirit,' protects cohesion proteins that hold chromosomes together in eggs.

Women are born with a lifetime stock of oocytes, about 7 million in the fetus and 1 million at birth, which remain paused for decades until ovulation. During this wait, paired chromosome copies can separate prematurely, leading to aneuploidy — wrong number of chromosomes —, the main cause of infertility and IVF failures. 'This creates huge problems at the chromosomal level, because they kind of wait for years in humans, which is insane in a way,' explains Paula Cohen, director of the Center for Reproductive Sciences at Cornell University.

In experiments with mouse and human cells, restoring Shugoshin via messenger RNA increased eggs with intact chromosomes from about half to nearly three-quarters. 'If you want to develop strategies to improve egg quality and create clinical ways to really help couples conceive, you need to understand what's going wrong at the molecular level,' says Zielinska.

Independent scientists, like Michael Lampson from the University of Pennsylvania, note that prior focus was on cohesin proteins, but protecting the remaining ones makes sense. Binyam Mogessie from Yale observes partial recovery and plans drug tests. Cohen warns it won't solve everything: 'This won't solve the problem for everyone... but we're much further along than just 10 years ago.' Ovo Labs plans a clinical trial to test the intervention in IVF, while another study in Nature Aging simulates aging in mouse eggs to probe failures.

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Split-scene illustration of UCSF mouse study: older mouse struggles in maze with poor hippocampal neural links due to FTL1; treated mouse excels with enhanced connections.
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UCSF study links iron-associated protein FTL1 to age-related memory decline in mice

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Researchers at the University of California, San Francisco report that higher levels of the iron-associated protein FTL1 in the hippocampus of older mice are tied to weaker neural connections and worse performance on cognitive tests. In the experiments, reducing FTL1 in older mice was associated with increased neuronal connectivity and improved memory performance, findings published in Nature Aging.

Researchers at UCLA have identified a protein that slows muscle repair in aging but enhances cell survival in mice. Blocking the protein improved healing speed in older mice, though it reduced long-term stem cell resilience. The findings suggest aging involves survival strategies rather than mere decline.

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Researchers have discovered that DNA in newly fertilized eggs forms a structured 3D scaffold before the genome activates, challenging long-held assumptions. Using a new technique called Pico-C, scientists mapped this organization in fruit fly embryos. A related study shows that disrupting this structure in human cells triggers an immune response as if under viral attack.

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Researchers at Marshall University report that microscopic particles found in the gut lumen—known as exosomes—differ between young and old mice and can influence metabolism and gut-barrier function when transferred between animals. The findings, published in the journal Aging Cell, suggest these particles may help drive biological changes associated with aging, though the work is preclinical.

Researchers have boosted strawberry fruit quality by increasing activity of a housekeeping gene called FveIPT2. The modification raised levels of anthocyanins and terpenoids for richer color, aroma, and nutrition without affecting plant growth, fruit size, or sweetness. The findings, published in Horticulture Research, challenge views on basic cellular genes.

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Researchers at Israel's Weizmann Institute of Science have determined that genetics explain about 50% of differences in human lifespan, far more than previously estimated. The finding, published in the journal Science, challenges earlier views that placed genetic influence at 20-25% or less. By analyzing twin data and filtering out external death causes, the team uncovered this stronger hereditary role.

 

 

 

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