I found a 2013 article that further establishes neuroprotection benefit from sex hormones. I'm posting it here because of the useful information in this thread from 2006. I really appreciate the wealth of knowledge and depth of insight in the conversation that has been happening on thisisms over the years.
Here is the excerpt from the recent article re hormones and ms, available in full text from pub med central.
Front Neuroendocrinol. Author manuscript; available in PMC 2013 April 4.
Published in final edited form as:
Front Neuroendocrinol. 2012 January; 33(1): 105–115.
Published online 2011 December 24. doi: 10.1016/j.yfrne.2011.12.001
Neuroprotective effects of estrogens and androgens in CNS inflammation and neurodegeneration
Rory D. Spence and Rhonda R. Voskuhl*
With estrogen’s ability to provide protection in a number of CNS disease models, much research has been focused on the mitochondria as a target of estrogens actions. Treatments with estrogens have a direct neuroprotective effect on mitochondria [16,55,95,96,97]. Estrogens have been shown to increase aerobic glycolysis, respiratory efficiency, ATP generation, Ca2+ load tolerance and act as an antioxidant defense . Furthermore, estrogens can alter pro and anti-apoptotic molecules that act on the mitochondria. For instance, estrogen can increase anti-apoptotic markers, bcl-2 and bcl-xl, while decreasing the pro-apoptotic marker bax in animal models of AD . Estrogen’s antioxidant properties also allow it to protect against reactive oxygen species from the mitochondria . It is important to note that the timing of estrogen administration is critical to ensure estrogens protective outcome as noted in the healthy cell bias of estrogen action hypothesis. If estrogens are administered too late in the disease they are not protective [17,94,124,156].
Currently, MS treatments have a primary focus on reducing inflammation. Given that MS is both an inflammatory and neurodegenerative disease, there is a need for neuroprotective treatments if one aims to fully halt the disease . Estrogens and androgens both have the potential to play neuroprotective roles in the treatment of MS. EAE studies with various estrogen and androgen treatments led to clinical disease protection, as well as protection from CNS inflammation, axonal loss, as well as demyelination. ER? ligand treatment was able to completely abrogate both early and late stages of disease. However, it is unlikely ER? ligand treatment could be used long term or in high doses since breast and ovarian cancers are mediated via ER? in humans [12,90]. ER? ligand and estriol treatments remain promising candidates for MS since they have the potential to be much safer due to either no, or relatively low, binding to ER? respectively [60,63,62,155]. In the EAE model, ER? ligand was able to ameliorate late signs of clinical disease while providing neuroprotection even in the presence of CNS inflammation [23,141]. Recent evidence suggests that ER? ligand may not only prevent demyelination, but also promote remyelination . However, since ER? ligand is does not prevent CNS inflammation, it would theoretically need to be given in combination with an anti-inflammatory agent in MS . Androgen treatment remains a candidate for male MS patients. While some anti-inflammatory effects of testosterone have been shown in EAE, direct neuroprotective effects have not been addressed. It remains unclear whether the protective effect of testosterone might be due to its conversion to estrogen in the CNS.