Estrogen, a Steroid Hormone

Our results extend previous observations describing estrogen’s neuroprotective effects. A previous study suggested that the sex hormones estrogen and testosterone worked differently as neuroprotective agents. It provided data for a role of testosterone as a neuroprotective hormone in neurons. When looking at how they regulate protease activity, their results show that testosterone and dihydrotestosterone inhibited calpain activation and the generation of the 17-kDa tau fragment, but did not work on caspase-3 activation and tau truncation at Asp421 as estrogen did.

Taken together, this indicated that estrogen and testosterone have independent pathways that mediate the neuroprotective effects of these sex hormones.

In short, we show that estrogen is neuroprotective in ONHAs and can inhibit caspase-3 activation and reduce tau cleavage, thereby preventing NFT formation. We also noticed that a 2-hour preincubation, like the 18-hour, was effective in reducing caspase-3 activation and tau proteolytic cleavage, although the longer preincubation was more beneficial. A previous study showed that the neuroprotective properties of estrogen and testosterone on hippocampal neurons with A?-induced neurotoxicity were effective not only when preincubated at 24 hours but also when preincubated for 2 hours prior to A? addition (Ferreira, 2007).

Based on our data, Tau plays an important role in the degeneration of the neural retina. Our data indicate that the delivery of sex hormones (estrogen) has potential therapeutic value and appears to target Tau and the caspase-3 pathway. Studying the pathogenesis of retinal Tau can increase our knowledge of vital mechanisms involved in neuronal and cellular degeneration.”

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