Myelin-producing ability?

Multiple sclerosis, Pathology of recurrent lesions

"Recent autopsy studies suggest that remyelinated shadow plaques located in otherwise intact white matter are the outcome of a previous single episode of acute demyelination."

What do I make out of this? Remyelinated shadow plaques, evidence of remyelination following acute demyelination. Demyelination occurred as being the outcome of a single episode. This observation that the remyelinated shadow plaques are located in intact white matter contradicts what someone would expect after the episode of acute demyelination. Would it not, white matter be affected by demyelination? Therefore the claim that it is intact, is not valid.

Whatever, what matters, at that moment is the occurence of demyelination, as single episodes of autoimmune attacks. Moreover, another point out of this statement is, that remyelination reported after such an attack indicates that the ability to produce new myelin sheaths is not lost, so what is destroyed during the single episode of acute demyelination, is the myelin itself, i.e. the product of the oligodendrocytes.

However, this finding dates at 1993, and since then …

"The findings also support experimental evidence that recurrent demyelination of the same area of white matter may be one of the factors underlying failed remyelination in multiple sclerosis."

The … the remark above was hasty, but for the sake of following the course of the thoughts developing i will leave it as is and revise it accordingly. What comes out of it is the recurrent demyelination of the same area of whte matter. Additive? Episode-after-episode? Failed remyelination? In what sense? Demyelination and remyelination competing against each other? Demyelinated axons are remyelinated and remyelinated axons demyelinate? Meaning that myelination itself is not lost, the ability of oligodendrocytes to produce and lay down myelin sheaths is not lost, and the actual progress of multiple sclerosis is determined as the result of a faster rate of demyelination than myelination. Or is it, that for designated areas of white matter the demyelinated axonxs cannot be myelinated again, the mylienating ability is lost. Completely? Forever?

That either, the myelin laying down capability or the myelin producing ability or both is impaired? Myelin-producing ability, functioning oligodendrocytes being present, is affected? Oligodendrocytes killed? Apoptosis?

New Research Challenges Pathogenesis of Multiple Sclerosis

"Findings from an autopsy study by Australian researchers question the
theory of
multiple sclerosis (MS) that holds that an autoimmune attack
on myelin is the inciting event for the disease
."

Australian researchers, led by Dr John W. Prineas, as it was referenced in ‘How does Multiple Sclerosis do its damage?‘ article, question whether autoimmune attacks are the starting points of multiple sclerosis. Whether demyelination occurred and observed, is a result of myelin destroyed by the autoimmune response, as being the primary cause of multiple sclerosis disease. But instead, claim that demyelination is a secondary effect, the myelin-producing ability is impaired first?

Oligodendrocyte precursor cells in the demyelinated multiple sclerosis spinal cord.

"This failure of remyelination appears, in many cases, to be due not to
the destruction of the local oligodendrocyte precursor population, a
source for new myelin-forming cells, but to the failure of the
precursor cells to proliferate and differentiate, at least in brain
lesions.
"

Remyelination ability lost as a result of the failure of oligodendrocyte precursor cells to proliferate and differentiate, at least in brain affected regions?

 

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