Posting this here because estradiol and testosterone are, like vitamin D, secosteroids that interact. It may be that the benefits being found in recent studies are the result of this interaction with calcitriol, the bio-active form of vitamin D. (I don't know that. I'm just speculating that this may be the case since I know all three are secosteroids and that they interact in various way.)
A presentation on Estradiol + Copaxone at the AAN meeting is getting a lot of press, but probably because Teva is promoting it. The same research group recently published a paper on testosterone alone, no DMD, which showed significant benefit. I would guess this is probably true for estradiol and ultimately, it may be true for calcitriol if as I suspect, the effect is somehow mediated by the interaction of the secosteroids.
Source URL: http://www.ncbi.nlm.nih.gov/pubmed/24634831
Journal Title: NeuroImage. Clinical
Journal Date: 2014
Journal Volume: 4
Journal First Page: 454-60
Abstract URL: http://www.ncbi.nlm.nih.gov/pubmed/2463 ... t=abstract
Article Title: Neuroprotective effects of testosterone treatment in men with multiple sclerosis.
Article Authors: Florian Kurth,Eileen Luders,Nancy L Sicotte,Christian Gaser,Barbara S Giesser,Ronald S Swerdloff,Michael J Montag,Rhonda R Voskuhl,Allan Mackenzie-Graham
Neuroimage Clin. 2014 Mar 6;4:454-60. doi: 10.1016/j.nicl.2014.03.001. eCollection 2014.
Neuroprotective effects of testosterone treatment in men with multiple sclerosis.
Kurth F1, Luders E1, Sicotte NL2, Gaser C3, Giesser BS4, Swerdloff RS5, Montag MJ4, Voskuhl RR4, Mackenzie-Graham A1.
1Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA ; Brain Mapping Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
2Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA ; Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
3Department of Psychiatry, Jena University Hospital, Jena, Germany ; Department of Neurology, Jena University Hospital, Jena, Germany.
4Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
5Department of Medicine, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute, Torrance, CA, USA.
Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease of the central nervous system. While current medication reduces relapses and inflammatory activity, it has only a modest effect on long-term disability and gray matter atrophy. Here, we have characterized the potential neuroprotective effects of testosterone on cerebral gray matter in a pilot clinical trial. Ten men with relapsing-remitting MS were included in this open-label phase II trial. Subjects were observed without treatment for 6 months, followed by testosterone treatment for another 12 months. Focal gray matter loss as a marker for neurodegeneration was assessed using voxel-based morphometry. During the non-treatment phase, significant voxel-wise gray matter decreases were widespread (p≤ 0.05 corrected). However, during testosterone treatment, gray matter loss was no longer evident. In fact, a significant gray matter increase in the right frontal cortex was observed (p≤ 0.05 corrected). These observations support the potential of testosterone treatment to stall (and perhaps even reverse) neurodegeneration associated with MS. Furthermore, they warrant the investigation of testosterone's neuroprotective effects in larger, placebo controlled MS trials as well as in other neurodegenerative diseases. This is the first report of gray matter increase as the result of treatment in MS.
Free PMC Article
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