How different is ms from other cns diseases?

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How different is ms from other cns diseases?

Postby bromley » Thu Mar 24, 2005 9:54 am

Dear all,

I would welcome any views on the following questions:

Many other diseases of the CNS involve cell / nerve death e.g. MND, Parkinsons, Alzheimers. MS when SP or PP is descibed in terms of the slow death of axons (nerve fibres). To what extent do these other diseases involve inflammation / the immune system?

What is the basis for the assumption that ms involves the immune system or is an auto-immune disease?

I suppose the difference with ms is that it affects teenagers / young adults whereas the other diseases genrally arrive in later life. Has this influenced the view of the research world that ms must be different from these other diseases?

Bromley
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Re: How different is ms from other cns diseases?

Postby Daunted » Thu Mar 24, 2005 12:07 pm

Well, not to be monomaniacal... but one common thread between Alzheimer's, MS, and Guillian-Barre, as well as some people with 'inflammatory OND [Other Neurological Disease]', is the demonstrated presence of Chlamydia pneumoniae bacteria in some people with the disease.

Hence for someone like myself, "in limbo" and diagnosed with "mild Guillian-Barre", "cryptogenic polyneuropathy", and "possible MS", the antibiotic treatment was the common thread that seemed a good option.

I would think research on the underlying causes of these diseases would also have to account for the presence of CPn, even if it is an "innocent bystander". (which I tend to disbelieve, but which certainly needs further research).
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Re: How different is ms from other cns diseases?

Postby NHE » Tue Apr 05, 2005 1:40 am

Bromley wrote:What is the basis for the assumption that ms involves the immune system or is an auto-immune disease?


To the best of my understanding, adoptive transfer plays a big role in the autoimmune theory of MS. Essentially, activated T cells which target proteins such as myelin oligodendroycte glycoprotein are transferred from one individual with MS or EAE to a naive individual. The immune system of the naive individual then develops its own targeted attack against the initial antigen producing MS/EAE in the naive individual.

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Postby BioDocFL » Tue Apr 05, 2005 7:26 am

I wonder if the transferred T cells may be after epitope-spreading has occurred in the first subject. Something abnormal in the first subject may have provoked an immune reaction, the abnormal target (ex. an improperly modified protein) was associated with normal proteins so the first subject's immune system started targeting the abnormal/normal combination and eventually even the normal proteins alone. The transfer of activated T cells may be primarily T cells that target the abnormal/normal combination or the normal proteins alone. I would like to hear how the researchers who transfer the T cells explain the possibilities that epitope-spreading may or may not have occurred.

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Re: How different is ms from other cns diseases?

Postby NHE » Wed Apr 06, 2005 2:50 am

Wesley,
I don't know if this will answer your question but I thought it might be helpful. While this is just one paper, these authors state that epitope spreading is not necessary for the development of EAE. I should note that this paper is freely available from the Journal of Immunology. If this doesn't address the issue you're asking about, then it would be great if you could clarify your question.
To determine whether relapsing or progressive EAE can occur in the absence of epitope spreading, we evaluated the course of disease in mice which possessed only a single myelin-specific TCR. These mice (transgenic/SCID +/+) exhibited a progressive and sometimes remitting/relapsing disease course in the absence of immune reactivity to multiple, spreading myelin epitopes.

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Postby treez » Wed Apr 06, 2005 5:53 am

Dear Bromley,

Sounding rather simple but I think you vaguely answered your own question. "inflammation"

Alzheimer's involves mild inflammation....studies have shown those that have taken antinflammatories for some time have a reduced risk of developing it.

Parkinsons involves inflammation in a specific part of the brain(substantia nigra).

I'm currently focusing on this inflammatory component. It would be fair to conclude if you could control the inflammation, you could control the disease.

I'm thinking the myelin and axon involvement is collateral damage due to an earlier immune response.

It is well known that the body has a tendency to "overreact" with it's inflammatory responses and clean up crews.

Hope I'm not off base with my hypotheses here

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katie45

Postby katie45 » Mon Apr 11, 2005 3:03 pm

treez, I don't think this "theory" is off base at all....I've been screaming this for years. The human body (in my opinion) does not attack itself. Simply because "they" cannot find the pathogen with the current testing available does NOT mean it isn't there.

One might wonder where commom logic was tossed out in favor of modern science. I believe the human body/brain has only so many ways to manifest a response to an invasion. Thus all the labels..fibro, Chronic fatigue syndrome (now there's a well thought out scientific label) MS, parkinsons etc,

I also believe many, if not all of these so called diseases are inflamatory responses.
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Re: katie45

Postby kareng7 » Thu Apr 28, 2005 3:35 pm

katie45 wrote:...I've been screaming this for years. The human body (in my opinion) does not attack itself. Simply because "they" cannot find the pathogen with the current testing available does NOT mean it isn't there...I believe the human body/brain has only so many ways to manifest a response to an invasion. Thus all the labels..fibro, Chronic fatigue syndrome (now there's a well thought out scientific label) MS, parkinsons etc...I also believe many, if not all of these so called diseases are inflamatory responses.


I'm new to all this, but I've been doing a lot of reading and katie45 has very eloquently summed up my beliefs/hypotheses. I do believe, however, that some sort of susceptibility of the human body is involved.

My husband has psoriasis, with psoriatic arthritis (he's on Enbrel--we may soon be a two-injection household. javascript:emoticon(':roll:')). The medical community is fairly certain they've identified genes that play a role in the manifestation of psoriasis. But that doesn't mean there isn't some sort of trigger.

Here's some totally theoretical stuff I've thought about with us. My husband swears he's allergic to cats, but that, when living with cats (which we do), he becomes tolerant of them. He's even been to an allergist who did the skin prick test and said, nope, no cat allergy. But when we visit folks with other cats, sure enough, he starts sneezing. Perhaps it's because of some other pathogen in a foreign environment. But perhaps, just perhaps, his body shifts its response from the typical allergic sneeze to a skin reaction (aka, psoriasis) in an effort to fight continual exposure to the specific allergens of the cats in our household, but when exposed to other cats, it reverts to the more common, perhaps "acute" symptom of respiratory congestion, like asthma. Allergy and inflammation are well-linked. Is it possible the body will shift from one inflammatory response to another, or other, more insidious one(s), in its effort to deal with an ongoing assault?

Back to pathogens. Here's another theory I'm chewing on. The concept that RRMS "becomes" progressive is so very much like how, if left untreated, syphilis will progress from sores (primary) to skin rashes and other intermediary symptoms (secondary) to CNS and cardiovascular involvement (tertiary). Of course, it's also not unlike the way the AIDS virus infects, then remains dormant for years, until it strikes and then progresses. If you think about it, the whole "HIV" vs. "AIDS" nomenclature is not unlike "Clinically Isolated Event," (which they say I have) vs. "Clinically Definite MS."

Viruses and bacteria are clever. I think the medical community underestimates their ability to survive, prevail, and adapt.

I could go on and on with these theories. Please either stop me or chime in!
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Re: How different is ms from other cns diseases?

Postby NHE » Fri Apr 29, 2005 6:27 am

katie45 wrote:I've been screaming this for years. The human body (in my opinion) does not attack itself.

This review (abstract posted below) discusses that nearly everybody has some autoreactive T cells. In most cases, folks with a healthy immune system will keep these autoreactive cells in check and keep them from proliferating. Unfortunately, for folks with an immune system that has gone awry in its ability to regulate itself, e.g., mutations or misregulation of important genes that control the apoptotic pathway, these autoreactive T cells can lead to diseases such as MS. This is not to say that some unknown infectious agent does not play a role in MS. It seems likely to me that there could be a pathogen, which through molecular mimicry (in effect one of its proteins is structurally similar to those found in myelin), triggers the initial formation of autoreactive T cells which are then not kept in check.

Walker, L.S. and Abbas, A.K. 2002. The enemy within: keeping self-reactive T cells at bay in the periphery. Nat Rev Immunol 2(1):11-19.

The remarkable capacity of the mammalian immune system to coordinate deadly attacks against numerous invading pathogens, yet turn a blind eye to self-tissues continues to fascinate immunologists. It has been clear for some time that immune cells capable of recognizing self-proteins exist in normal individuals without seemingly causing harm. The 'peripheral tolerance' mechanisms that keep these cells in check are the focus of intense research, not least because defects in these pathways might cause autoimmune diseases. In this review, new developments in our understanding of peripheral tolerance are discussed.

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