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Petr75 wrote:2017 Jul 18
Glucocorticoid-associated blood glucose response and MS relapse recovery
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5515601/

..Our data provide important insights into 1 possible mechanism that impaired glucose tolerance may be contributing to increased progression among patients with MS, even those without a confirmed diagnosis of diabetes.

Great finding!! it also fits in the global picture. I really think they are on the right path.

... they tested 200 fragment mixtures, each containing 300 billion varieties. The two fragments with the strongest effect turned out to be part of a human enzyme called guanosine diphosphate-L-fucose synthase, which helps cells remodel sugars ...

Actually, it is CD20 b cells that cause an inflammatory cascade initially, resulting in demyelination and abnormal re-myelination. New evidence has identified that B cells in persons with MS activate T-cells to become pathogenic so the result is many T cells are found in some of the larger lesions and remain there

It actually makes sense that in Ms part of the pathology is that B cells activate T-cells to become pathogenic because in some types of immunizations like tetanus for example the B cells Ferry the toxoid to the T cell to train the T-cell to recognize the toxoid as something to create an antigen against and therefore you have protection against the tetanus toxoids

Of note memory B cells are actually implicated in Guillain-Barre syndrome which is another demyelinating disease

https://www.ncbi.nlm.nih.gov/m/pubmed/28284328/

Memory B cells in Guillain-Barré syndrome.

The topic - I wonder if there is a link ?:

http://www.neurology.org/content/61/10/ ... .large.jpg

and


https://fityou.cz/wp-content/uploads/20 ... -cukru.jpg