More Ideas About Multiple Sclerosis:

Although scars are so important in MS that they are the basis of the word "sclerosis", almost no attention is given to the cellular and/or molecular causes of the scars, nor of treatment of MS with drugs that either inhibit scar formation, or stimulate removal of the mixture of myofibroblasts and more-tightly-packed-than-usual type I collagen fibers.

Scar formation has been an active subject of research, although as regards skin and internal organs, and not so much as regards nerves and the interior of the brain.

The consensus has developed that scars consist of abnormally strong contractility of mesechymal cells (called "myofibroblasts") mixed with type I collagen fibers that are packed together more tightly than in undamaged tissues. Incidentally, some glial cells tie with scar fibroblasts as the cells which exert the strongest traction on rubber sheets (personal observation, that has always puzzled me; maybe oligodendrocytes are strong?)

Will scars always form where oligodendrocytes have died, been killed, or been damaged?

Does MS cause death of oligodendrocytes, or merely damage the myelin they produce?

Can oligodendrocytes be protected? Can oligodendrocytes regenerate?

Does MS cause changes in strengths of traction forces exerted by oligodendrocytes?

Questions like this are not even being asked, nor speculated about, much less funded.

If oligodendrocytes are killed (for any reason) do their nerve axons cease propagating action potentials? Or is formation of scar tissue what blocks action potentials?

Does MS paralysis results from death of oligodendrocytes?

These kinds of questions seem not to be asked.

Do they know the differences between T and B lymphocytes? What assumptions do they seem to make about causes of antibody binding site shapes? ...and about self-tolerance?

Can "microfluidics and "Chip" technology be adapted to test effects on MS of changed combinations and differing ratios of amino acids in random co-polymers like Glatiramer?


Can microfluidics and "chip" technology be used to compare effectiveness of alternatives to glatiramer (random peptides of lysine-alanine-tyrosine-glutamic acid)?

Random copolymers could also be studied by X-ray crystallography and electron crystallography. Another approach would be to bind gadolinium atoms to co-peptide polymers, inject these into MS patients before or during Magnetic Resonance Scans, to find out whether glatiramer or comparable substances become localized at places where MS is causing brain damage. (Given that damage is concentrated in ellipsoidal foci.)


I just realized that GLAT is the acronym for GlutamicAcid Lysine Alanine Tyrosine

If these are the 4 most numerous amino acids in myelin basic protein, then let's find out.

Or could they just as well have polymerized Aspartic Acid, Arginine, Glycine, and Phenyl-Alanine? (Those are the 4 amino acids with structures closest to GLAT.)

Protein conformations result from sequences of amino acids, and only secondarily from relative amounts of amino acids. One site suggests that the relative amounts might be 40% Alanine, 13% Glutamic acid, 30% Lysine, and 9% Tyrosine (which adds up to 92%)

Please try to find out the relative amounts, and whether % are by weights or by relative numbers of amino acids. And is it even known whether relative amounts matter in treatment?

Tens of thousands of people just like you are dying in misery for lack of the kind of intense speculation that Watson and Crick focused on the question of DNA structure.

Questions have answers, and there is no good reason why you can't find those answers.


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