New research advancements in the treatment of premature ovarian failure

Scientific Director of the Meharry Center for Women's Health Research and a team of researchers from the University of Texas Medical Branch and the University of Saskatchewan have recently discovered that the gene mutation believed to be a possible cause of premature ovarian failure may be corrected when an adenovirus compensating for the mutated gene is introduced. Findings were reported in the recent issue of Molecular Human Reproduction.

Premature ovarian failure affects 1% of women worldwide and occurs in young women between the ages of 15 and 25. When a woman has premature ovarian failure, her ovaries stop producing eggs and estrogen resulting in infertility and early menopause.

Dr. Ayman Al-Hendy, who is also a professor and vice chair of the Department of Obstetrics and Gynecology at Meharry Medical College said, “The objective of our study is to develop a gene therapy approach for the treatment of this type of infertility. This is the first published work since the discovery of the Finnish C566T mutation that examines what happens at the cellular level when an adenovirus expressing the normal gene is introduced in the presence of the gene mutation.”

Al-Hendy said he and his team are encouraged by the findings and hope that future studies will show that once the mutation is corrected with the replacement of a healthy gene, the ovaries can be restored to normal functioning levels including ovulation and the production of estrogen.

First discovered in 1995 the gene mutation known as the C566T blocks the normal function of the follicle stimulating hormone receptor and prevents the normal development of ovarian follicles and eggs in females. Women who have premature ovarian failure usually cannot become pregnant with their own biological children. They often receive hormone replacement therapy to alleviate menopausal symptoms.

“You can imagine how devastating this condition is for the young woman who has it. While a cure or treatment option is several years away, findings like the one in our study is encouraging and promising” said Dr. Al-Hendy.

More research is still needed and work is currently underway to confirm the in vitro data in appropriate animal models before clinical trials in women begin.

The study is published this month in the specialized medical journal Molecular Human Reproduction. The manuscript is titled, “Toward gene therapy of primary ovarian failure: Adenovirus expressing human FSH receptor corrects the Finnish C566T mutation.” In addition to Al-Hendy, co-authors of the study include the following: Moshen Ghadami also from the Center of women health research, Meharry Medical College, Salama A. Salama, Nilufar Khatoon, Rebecca Chilvers, Manubai Nagamani from the OB/GYN department, University of Texas Medial Branch at Galveston (UTMB) in Galveston, Texas and Jorge Chedrese, Department of OB/GYN and reproductive Sciences, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. For more information, please contact Janet M. Caldwell, by phone: 615.327.6851 or email: [email protected]

Meharry Medical College is the nation's largest private, independent historically black academic health center dedicated solely to educating minority and other health professionals. The College is particularly well known for its uniquely nurturing, highly effective educational programs; emerging preeminence in health disparities research; culturally sensitive, evidence-based health services; and significant contribution to the diversity of the nation's health professions workforce. Diverse Issues in Higher Education's ranking of institutions annually lists Meharry as a leading national educator of African Americans with M.D. and D.D.S. degrees, and Ph.D. degrees in the biomedical sciences.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post
You might also like...
Research suggests that ORF6 is a major SARS-CoV-2 innate immune antagonist