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OK I'll stop being facetious. This seems to be a very significant discovery indeed. It should make the use of EAE (the MS mouse model) unnecessary, for the most part, and cause drug research to stop using it. Do spinal taps of MS patients to have great value after all?

The cause of MS should be within our grasp. Once the cause is known, a cure (if it exists) can be found.

Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demyelination and neurodegeneration throughout the CNS, which lead over time to a condition of irreversible functional decline known as progressive MS. Currently, there are no satisfactory treatments for this condition because the mechanisms that underlie
disease progression are not well understood. This is partly due to the lack of a specific animal model that represents
progressive MS. We investigated the effects of intracerebroventricular injections of cerebrospinal fluid (CSF)
derived from untreated primary progressive (PPMS), secondary progressive (SPMS), and relapsing/remitting
(RRMS) MS patients into mice. We found discrete inflammatory demyelinating lesions containing macrophages,
B cell and T cell infiltrates in the brains of animals injected with CSF from patients with progressive MS. These
lesions were rarely found in animals injected with RRMS-CSF and never in those treated with control-CSF. Animals
that developed brain lesions also presented extensive inflammation in their spinal cord. However, discrete spinal
cord lesions were rare and only seen in animals injected with PPMS-CSF. Axonal loss and astrogliosis were seen
within the lesions following the initial demyelination. In addition, Th17 cell activity was enhanced in the CNS
and in lymph nodes of progressive MS-CSF injected animals compared to controls. Furthermore, CSF derived
from MS patients who were clinically stable following therapy had greatly diminished capacity to induce CNS
lesions in mice. Finally,we provided evidence suggesting that differential expression of pro-inflammatory cytokines
present in the progressive MS CSF might be involved in the observed mouse pathology. Our data suggests that the
agent(s) responsible for the demyelination and neurodegeneration characteristic of progressive MS is present in
patient CSF and is amenable to further characterization in experimental models of the disease.

From the paper,

Demyelination precedes axonal loss and glial scar formation.

Progressive MS-CSF treatments altered the expression of immune-system
related genes in the mouse CNS.

Progressive MS-CSF treatments enhanced Th17 cell activity in the mouse
CNS and in its periphery

.

CSF-induced brain lesions are drastically reduced by clinical treatment and
correlate with patient CSF levels of pro-inflammatory cytokines

.

Something got into the human CSF that caused MS in the mice. Not model MS. Real MS. MS is not contagious to mice, that we know of, though do we really know? It suggests to me an environmental cause.

MS seems to follow the CSF. Progression seems to be related to spinal lesions. MS seems to migrate from brain to spine. Spinal lesions are usually, but not always, found in progressive MS.

These results look to me like they suggest serious genetic involvement, which we already knew. But do genes only cause susceptibility, or are they the direct cause? Compare plain mouse DNA to MS-mouse DNA before and after? Compare MS-mouse DNA to MS-human DNA?

Something takes a while to migrate out of the brain, except in "PPMS" it's immediate. It seems to stop most remissions once it's out.

Do we have to keep using the term "irreversible"? Or are we just quitters?

Cross-posting this to the general discussion forum. There are a number of topics on this paper on TiMS. Perhaps they should be combined and moved there?