James M. Flynn

TL;DR: In this paper, 17beta-estradiol (17beta-E2) was shown to act as a positive regulator of the survival signal transduction pathway, which in turn acts to stabilize DeltaPsi(m), attenuating the extent of depolarization of mitochondrial membrane potential in the face of acute oxidative stress.

TL;DR: The results support the conclusion that the intrinsic bioenergetic capacities of presynaptic nerve terminals are maintained in these symptomatic AD mouse models.

TL;DR: It is proposed that estrogen-induced activation of ERK2 acts to protect cells from acute oxidative stress via an ERK-independent mechanism and regulates MMP in humans lens epithelial cells.

TL;DR: Polyol accumulation promotes mitochondrial membrane depolarization and the decrease in Deltapsim is prevented by prior addition and co-administration of Sorbinil or estrogen with Gal, which supports the theory that with Gal plus estradiol-treated cells, at a given intracellular polyol load, a larger portion of the mitochondrial population retains Deltapim, and hence continues to function relative to Gal-treated Cells.

TL;DR: No clear evidence is observed that CR as it is currently practiced in humans delays immune aging related to telomere length or T cell immunosenescence markers.