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I don’t think it’s that settled at all, certainly not in 1965. Prineas in 2001 showed that MS progression may occur in the absence of immune cells and inflammation, for example [0], and people have complained of progression even when taking extremely strong immunosuppressants.

While involvement of the immune system seems likely, and certainly most treatments target the immune system, I don’t think causality has been rigorously demonstrated. It has however been a few years since I looked into it.

As an aside, ISTM quite likely that there may be several causes for MS.

[0] https://pubmed.ncbi.nlm.nih.gov/11706971/

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I wonder how often science gets derailed simply because people are in the habit of expecting a single answer to their questions. We know that car accidents cause lacerations, although there are plenty of cases that happen in the absence of car accidents. Isn't it possible that MS is a symptom with multiple possible causes, any of which could set off a vicious cycle of nerve degeneration?

The scientists don't get derailed, but I get too many forwarded articles with silver bullets. One of my friends suggested intentionally getting stung by bees. This is magical thinking for a complex illness.

On the other hand, tecfidera had as the active ingredient a chemical I can buy from alfa aesar for $22 a liter. There's a lot of things that no one has studied yet I guess, for better and worse.

> Prineas in 2001 showed that MS progression may occur in the absence of immune cells and inflammation

MS researcher here. MS as an autoimmune attack is largely settled in mainstream neuroscience. The paper you cited does not show what you said it does. From the paper: > restricted largely to short segments of disrupted myelin located within linear aggregates of microglial cells

The paper is interesting because it shows that demyelination is happening in lesions that we thought were inactive, but actually do contain microglia and macrophages (immune cells) eating myelin (i.e. an autoimmune --immune system attacking self-- attack). The paper is paywalled but I but you can read it on sci-hub (https://sci-hub.scihubtw.tw/10.1002/ana.1255) Although just reading the abstract says the opposite of what you are claiming, the entire thing is about microglia and macrophages contributing to lesions that the researchers thought were inactive.

OK. I might be quoting the wrong paper, and I’m not a researcher, but I remember clearly that he found a case (14yo girl IIRC) who died during an attack, and there was no immune activity at the site of at least one of the lesions.

If I’m wrong about this then I will accept it, I don’t have an axe to grind.

MS is a catch all. Multiple causes can result in demyelination even if the mechanism is the immune system. You have MS if you have demyelination products detectable in your spinal fluid and have lesions on the spinal cord. Whether it's a genetic, environmental, or some other underlying condition clearly varies, for instance the version that I have is almost certainly genetic because of family history but plenty of other people get it with no family history.

But I think people are pretty sure that certain B cells are the easiest to interrupt culprit, my current medication literally just kills a specific B cell and that treatment last six months. Take from that what you will.

_Causality_ is unlikely to be demonstrated until a direct cause is known, and for a complicated illness like MS, it is likely to be a variety of factors, an active and changing area of research.

That in itself doesn't in any way mean that MS wouldn't be classified as autoimmune, however. If there is a high degree of immune system involvement, then it is generally classified as autoimmune, or immune-mediated. And that had been demonstrated. Such as in this [0] paper.

[0] https://doi.org/10.1016%2Fj.febslet.2014.04.007

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