Read More at Fight Aging! Researchers here describe an interesting approach to slowing aspects of neurodegeneration that contribute to, among other things, female reproductive aging. That is the focus of this paper, but numerous other aspects of the aging brain are also involved. IGF1 is well studied in the context of aging, and manipulation of the signaling pathways linking insulin, IGF1, and growth hormone has been shown to extend life span in a number of species. Where we can make direct comparisons between mice and humans, such as between growth hormone receptor knockout mice and humans with Laron syndrome, the effects are nowhere near as large. Suppression of growth hormone signaling can extend life by 70% or so in mice, but Laron syndrome doesn’t appear to make humans live meaningfully longer. Many approaches to slowing aging have much larger effects…
Oocyte Mitophagy in Reproductive Aging
Read More at Fight Aging! In many species, aging of the female reproductive system occurs more rapidly than is the case for other parts of the body. This is one of a few biological systems subject to what appears to be premature aging, relative to other organs. Other examples include the thymus, which atrophies well before late life. Researcher here suggest that mitochondrial quality control, the process of mitophagy, is involved in the aging of oocytes to a great enough degree that upregulation of mitophagy may delay female reproductive aging. Women’s reproductive cessation is the earliest sign of human aging and is caused by decreasing oocyte quality. Similarly, C. elegans’ reproduction declines in mid-adulthood and is caused by oocyte quality decline. Aberrant mitochondrial morphology is a hallmark of age-related dysfunction, but the role of mitochondrial morphology and dynamics in reproductive…
Germline Stem Cells in Ovaries and Female Reproductive Aging
Read More at Fight Aging! In today’s open access paper, researchers discuss the evidence for the existence of germline stem cells in the ovaries, responsible for maintaining fertility in the usual manner of stem cells, by generating daughter cells that replace losses and ensure function. Is ovarian aging, leading into age-related infertility, much accelerated over the aging of other organs in our species because this stem cell population loses function more rapidly than those in other tissues? That is a reasonable hypothesis, and some of the possible mechanisms are discussed. That overies are a hypoxic environment to begin with, and that supply of oxygen and nutrients does tend to decline with age for a range of reasons, is one of the more intriguing ideas. A number of groups, including a few biotech startups in the growing longevity industry, appear to…