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Practical recommendations are presented for integrating these safe and well-tolerated orthomolecular nutrients into a comprehensive dietary supplementation program for brain vitality and productive lifespan.
The entire article is available free in pdf format. There's a small segment on MS and a nice table at the very end with a list of supplements/possible dosages.
INTERPRETATION: Our data supports a mechanism whereby reduced ATP production in demyelinated segments of upper motor neuron axons impacts ion homeostasis, induces Ca2+-mediated axonal degeneration, and contributes to progressive neurological disability in MS patients.
If you wonder why I emphasized the Ca2+ mediated axonal degeneration, it's because
The hormone plot thickens. Seriously though, it does seem that it might be worthwhile to pay attention to mitchochondrial degeneration in MS. The first article I posted had some MS specific references. This more recent information ties it to axonal degeneration and progressive disability in people with MS.
The axon may well be able to function for many years due to these adaptive mechanisms but we propose that eventually, despite antioxidant defences, free radical damage will accumulate and mitochondrial function will become compromised. ATP concentration within the axon will decrease and the effect on axonal function will be profound.
The actual cause of cell death could be due to a number of mechanisms related to mitochondrial dysfunction including failure of ionic homeostasis, calcium influx, mitochondrial mediated cell death or impaired axonal transport. Whatever the cause of axonal loss our hypothesis is that mitochondria are central to this process.
And this one, the role of mitochondria in MS doesn't really say that much but it does seem to reinforce the hypothesis and emphasizes early neuroprotection.
Quote:
The recognition that various mitochondrial mechanisms are involved in the pathogenesis of multiple sclerosis leads to therapeutic considerations, re-emphasizing the importance of early neuroprotection in combination with the approved means of immune modulation.
The mitochondria stuff interests me as "mitochondrial myopathy" was one of the diagnoses that was considered in my case.
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) an important update on this topic.
Seriously though, it does seem that it might be worthwhile to pay attention to mitchochondrial degeneration in MS. The first article I posted had some MS specific references. This more recent information ties it to axonal degeneration and progressive disability in people with MS.
