Jon Nilsen

TL;DR: Significant mitochondrial dysfunction occurs early in AD pathogenesis in a female AD mouse model and provides a plausible mechanistic rationale for the hypometabolism in brain that precedes AD diagnosis and suggests therapeutic targets for prevention of AD.

TL;DR: The impact of clinically used progestogens and developing selective PR modulators for targeted outcomes in brain is a critical avenue of investigation as the non-reproductive functions of PRs have far-reaching implications for hormone therapy to maintain neurological health and function throughout menopausal aging.

TL;DR: Not only was MPA an ineffective neuroprotectant but it attenuated the estrogen- induced neuroprotection when coadministered, and the role of MAPK activation in neuroprotection by ovarian steroids was addressed.

TL;DR: A mechanism of E2-induced neuronal survival by attenuation of excitotoxic glutamate [Ca2+]i rise via increased mitochondrial sequestration of cytosolic Ca2+ coupled with an increase in Bcl-2 expression to sustain mitochondrial Ca2- load tolerance and function is provided.

TL;DR: It is demonstrated that 17β-estradiol (E2) and progesterone (P4) treatment of hippocampal neurons attenuated the excitotoxic glutamate-induced rise in intracellular calcium concentration, and nuclear ERK induction by ovarian steroids is predictive of the neuroprotective effects of estrogen and progestin treatments, revealing a hitherto unrecognized divergence of progest in signaling through the src/MAPK pathway.