title: Selected enquiries into the causation of premature ovarian failure.
abstract: In most species, reproductive senescence can be explained in the same general terms as physiological senescence. In fact, in some species rapid physiological senescence occurs on the completion of reproduction. The programme in women is unusual in that ovarian function comes to a relatively abrupt halt at 45-50 years of age, when the impact of somatic senescence on most other functions is minimal. Early reproductive senescence has been reported in other species (chimpanzees, macaques and toothed whales) but it is more attenuated and less abrupt. The proximate cause of physiological menopause seems to be oocyte depletion, but less obvious neuroendocrine changes precede or result from the gradual loss of oocytes. This is not surprising as many age-specific processes are controlled by hormones. Hormones provide a way for an animal to co-ordinate the ageing of different tissues. The failure to comprehend completely the reasons for the biological uniqueness of women makes the study of the more extreme examples of premature ovarian failure an important exercise. The premature loss of ovarian function in certain eukaryotic women highlights the role of those special maintenance and repair systems that must be functional in the selection process for healthy germ cells. The purpose of this article is to indicate selected areas of clinical and basic investigation that may provide clues to the mechanisms of untimely ageing of the human ovary. Studies of those human extremes with premature loss, or extended ovarian function, may provide critical insights into the unique discordance between somatic and reproductive senescence that is characteristic of normal women.
authors.affiliation: Department of Obstetrics and Gynecology, Medical College of Georgia, Augusta, Georgia, USA.
authors.forename: Paul G
authors.initials: PG
authors.lastname: McDonough
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D004303:Dosage Compensation, Genetic; D005260:Female; D005600:Fragile X Syndrome; D006801:Humans; D008593:Menopause / Q000502:physiology; D008875:Middle Aged; D008938:Mitosis; D009134:Muscular Atrophy, Spinal / Q000150:complications; D009154:Mutation; D009223:Myotonic Dystrophy / Q000150:complications; D009865:Oocytes / Q000502:physiology; D006080:Ovarian Follicle / Q000196:embryology; D010053:Ovary / Q000196:embryology / Q000502:physiology; D016649:Primary Ovarian Insufficiency / Q000209:etiology* / Q000235:genetics; D011962:Receptors, FSH / Q000235:genetics
chemical_list: D011962:Receptors, FSH