Ovarian aging, infertility and cancer - understanding the role of mitochondria in ovarian senescence and implications in health and disease for individualized risk prediction and treatment

Not all women are born equal.

Even if the pool of ovarian follicles first formed in the ovaries is similar in size, some women will run out of eggs much faster than others, through mechanisms that are mostly unknown.

Ovarian aging occurs in all women, even in healthy individuals, with end of ovarian function and onset of menopause around the age of 50.

This indicates that the ovary ages faster than any other organ of the body, but the specific rate of ovarian aging differs among individuals and will determine how long the woman will be fertile and also the age at which she will develop menopause.

Premature ovarian aging is observed linked to genetic conditions; Turner syndrome, BRCA mutation carriers, among others.

Also, women that receive chemotherapy for treatment for cancer, accelerate their ovarian aging and often become infertile and develop premature menopause, with multiple negative health implications. We wish to investigate the molecular mechanisms behind the inter-individual differences in ovarian aging.

At our center for reproductive medicine patients are followed due to a risk for infertility and for premature menopause.

The prospective clinical cohorts are followed through sequential measurements of ovarian reserve biomarkers, clinical data and biobanked ovarian tissue samples, and the data will be available for this investigation. This study would be of outmost importance for both cancer survivours and women suffering from early menopause.