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Remyelination can be extensive in multiple sclerosis despite a long disease course 21 April 2007

Patani R, Balaratnam M, Vora A, Reynolds R. Department of Cellular and Molecular Neuroscience, UK MS Tissue Bank, Division of Neuroscience, Imperial College London, Charing Cross Hospital Campus, London, UK.
Experimental studies using models of multiple sclerosis (MS) indicate that rapid and extensive remyelination of inflammatory demyelinated lesions is not only possible, but is the normal situation. The presence of completely remyelinated MS lesions has been noted in numerous studies and routine limited sampling of post mortem MS material suggests that remyelination may be extensive in the early stages but eventually fails. However, visual macroscopic guided sampling tends to be biased towards chronic demyelinated lesions.

Here we have extensively sampled cerebral tissue from two MS cases to investigate the true extent of remyelination. Sections were cut from 185 cerebral tissue blocks and stained with haematoxylin and eosin (H&E), luxol fast blue and cresyl fast violet (LFB/CFV) and anti-myelin oligodendrocyte glycoprotein, human leucocyte antigen-DR (HLA-DR) and 200 kDa neurofilament protein antibodies. Demyelinated areas were identified in 141 blocks, comprising both white matter (WMLs) and/or grey matter lesions.

In total, 168 WMLs were identified, 22% of which were shadow plaques, 73% were partially remyelinated and only 5% were completely demyelinated. The average extent of lesion remyelination for all WMLs investigated was 47%. Increased density of HLA-DR(+) macrophages and microglia at the lesion border correlated significantly with more extensive remyelination.

Results from this study of two patients with long standing disease suggest that remyelination in MS may be more extensive than previously thought.

Source: Neuropathol Appl Neurobiol. 2007 Apr 18

TonyJegs,

Do you know what may be responsible for the remyelination? Is it because of something or the lack of something that causes the nerves to remyelinate?


gwa

-gwa

Remyelination in MS is more extensive indeed. This fact was continuously ignored in last couple of decades because of contradiction with mainstream ideas which served certain interests.
This study could be considered as one of signs of turning back to human MS from EAE in rodents. Of course the study is very small; expect that real numbers of remyelination will be slightly less but still impressive.
This study was probably based on ‘fresh’ brains from local source, why they have such opportunity to study them extensively. Usually when you deal with samples from any brain bank your possibility to analyze them is more limited.
The main source of remyelination is inactive oligodendrocytes which are located within the area of lesion. You can name them as ‘sleeping cells’. Primary function of these OL is to participate in physiological de-/remyelination on demand. In case when the number of these ‘reserve’ OL is inadequate to satisfy the demand, other OL will come from periventricular space. In case of MS lesion, or other WM damage, when lots of OL are whipped out, additional help comes from stem cells arrived through open BBB.

I would like to remind you that our body has a tremendous power of healing. In case of MS the possibility to ‘fix it up’ is much better compare to other neurodegenerative disorders, that why MS is my favorite. If you are able to control all stages of events before relapse, during relapse and right after it is possible to achieve excellent results, especially at early stages of disease, when treatment is more effective (note: of course you need to understand it completely).

Kind regards,
Tony

_________________
"All truth passes through three stages.
First it is ridiculed.
Second it is violently opposed.
Third it is accepted as being self-evident."
Schopenhauer

Hi Tony

Please can you elaborate on your inspiring words (above)?

Thanks

Ally