Mitochondria, Estrogen and Female Brain Aging
This article details the potential sequence of pathological events occurring at the mitochondrial level during aging and «the critical time period» of decline in estrogen (E2) in female brain.
During the premenopause, high levels of estrogen are paralleled by a normal mitochondrial activity with a balanced redox homeostasis and a high brain energy metabolism. At the beginning of the reproductive senescence, or perimenopause, a decrease of estrogen levels is accompanied with an increase of oxidative stress (ROS levels) and, consequently, hypometabolism.
During aging, alterations of the mitochondrial membrane lipid profile are also reported. Cells possess compensatory mechanisms, as antioxidant defenses, to keep the system in balance. In case the compensatory system is exhausted, metabolic impairments may occur, such as a decrease of ATP levels, glucose hypometabolism and mitochondrial respiration (e.g., cytochrome c oxidase (COX) activity) as well as myelin impairments.
In parallel, an increased expression of genes involved in fatty acid oxidation and the ketogenic pathway were reported as an alternative fuel for cells. The “critical period” (represented by the blue arrow) indicates a fast drop of estrogen levels in a relatively short time period, suggesting a period of women’s life where they are more vulnerable and more likely to develop age-related brain disorders such as Alzheimer’s disease (AD).
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