mTOR Signaling and Menopause

Researchers are digging in to some of the proximate mechanisms that lead to menopause, and making some progress by the looks of it. This is a good example of the general approach to aging taken by the research community: start at the end stage manifestation of dysfunction, such as menopause, and work backwards through layers of metabolic changes in search of causes. These changes are reactions to cellular and molecular damage that is fairly well described at this time. Researchers have a good catalog of the fundamental differences between old tissues and young tissues, but for most outcomes in aging there is no good understanding in detail of exactly how this damage spirals out to produce the observed late stage results.

So how to go about filling this gap in understanding? Instead of trying to fix the damage and working forwards to see the results, researchers follow a strategy of working backwards from the end stages. The final state of knowledge will be the same, but this approach is far less likely to produce meaningful treatments: applications of partial knowledge of the late stages of disease leads to efforts to manipulate the operation of a complex system in order that it runs less poorly when damaged. It is patching a failing machine, hard, expensive and doomed to failure. Compare that with treatments that remove the damage: much simpler, and more likely to be effective. If your engine rusts, you remove the rust every now and again, not rebuild the engine to work slightly better while rusting into uselessness.

Some women can have successful pregnancies at the age of 50, whereas other are unable to get pregnant when they are 30. Researchers are not yet able to fully explain such differences. One factor is that the onset of menopause is influenced by the point at which the uterus runs out of eggs to release. A recent [study] sheds light on the mystery of the biological clock that governs fertility. Just as newborn infants require nurturance in order to survive, eggs in the uterus need nourishment and support from the granulosa cells of the primary follicle. According to the latest [discovery] a signaling pathway in these cells plays a key role in enabling immature eggs to survive.

The mTOR signaling pathway in the granulosa cells is necessary for activating expression of the kit ligand growth factor, which subsequently binds to the c-kit receptors of eggs and determines their fate. "This mechanism permits the granulosa cells to decide when eggs will begin to grow and when they will die. In that sense, they serve as a kind of biological clock that monitors the onset of menopause." Researchers believe that the discovery will point the way to interventions that stimulate the growth of eggs that have been unable to mature.



Is it possible to restore the youth and beauty of women independent of fertility?

Posted by: Abelard Lindsey at October 29th, 2014 9:37 AM

Interesting that mTOR is again indicted as a driver of aging.

A couple of possibly relevant recent findings that seem to implicate the immune system (inflammation, IL-1) and telomeres (all probably one big loop) -

"Slowing The Biological Clock, Tel Aviv University Study"

"Girls under stress age more rapidly, new study reveals"

Posted by: Lou Pagnucco at October 29th, 2014 11:53 AM

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