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First of all, Fingolimod is a known active principle, an immune-modulator, which works theoretically modifying the behaviour of the Sphingosine-1-phosphate lipids, and in turn, the behaviour of b-cells and T-cells. But its action could be more than that.
The interesting connection is that Sphingosine-1-phosphate also modulates the Angiogenesis. Therefore a disregulated sphingosine system is expected to produce an unexpectedly wrong vascular system (https://www.wjgnet.com/1949-8454/full/v1/i10/291.htm)
We also know that there is some kind of mysterious substance in the MS patient's CSF that kills neurons. Probably is a high concentration of a substance known as ceramides (https://academic.oup.com/brain/article/ ... 71/2848013)
Guess where those ceramides come from? From the Sphingosine lipid system: https://link.springer.com/article/10.10 ... 010-8128-4
Maybe everything is connected. A wrong Sphingosine system could produce at the same time the venous problems found in CCSVI and the death of oligodendrocytes and demyelination found in NAWM (http://www.jbc.org/content/285/19/14134.short). After this first stage of damage is done, the BBB breaks down and macrophages enter the CNS to clean up the mess, producing the MS lesions, which is only the last part of the process.
What do you think?
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