How do different modulating drugs like avonex, betaseron, or rebif effect remyelination capacity that is lessened by chronicity?

[MRF_Justine]

Please see this recent article "Remyelination capacity of the MS brain decreases with disease chronicity" http://ow.ly/dO7D

I have a question from someone on Twitter about "how the different modulating drugs like avonex or betaseron or rebif and how they effect the remyelination capacity that is lessened by chronicity."

[MRF_Justine]

Thanks for the further clarification on the drugs for the different types of MS.

Laura -- No offense was taken. My access to the scientists is rather limited since they are all busy in their labs. I will bring up the question to the COO, Rusty Bromley, later today. Then I'll post his answer here.

[Lulu54]

Justine - didn't mean to sound like a smart aleck in my reply - I'm just wondering if you have access to many of those brilliant scientists hard at work on the remyelination question.  They could probably clear this question up for you in no time at all.

Jen is right about the SPMS dx - I probably am more SPMS than RRMS, even though my problems aren't severe, I seem to not had any remissions in this past year.  I have remained the same or perhaps worse. Tysabri is sometimes used in SPMS, but I'm not sure under what guidelines it can be rx'd,

If you find any extra neurons, you know there's a  whole bunch of people here willing to take them off your hands!

L

[jensequitur]

As far as I know, SPMS is usually diagnosed when the person stops having relapses.  After that point, there's no reason to be on the CRABs, as they are specifically to prevent relapses.  Another hallmark of SPMS is that the lesions stop remyelinating...  meaning that there is no remission.

However, neuros seem really leery of diagnosing anybody with SPMS.  I know several people who sound like SPMSers to me, but they're still on the CRABs.  

Obviously there's still a lot of research to be done on this!

[Lulu54]

justine -
I think that's part of the mystery - at least the copaxone I am on - it works to slow the number of relapses, but they're not sure why or how it works.  

Isn't there someone in a nearby cubicle you could ask and see if they know the answers to all of our questions?

L

[Ufrustrated2]

kayaking!! sounds great. did many of that and diving in the monterey bay area. indeed, do ship them.

maybe i can glue them back the sheath somehow. ;-)  enjoy the kayaking, such a fun way to "chill" and enjoy the day.

[MRF_Justine]

Thanks so much Laura and Jen for all this information. This is really interesting to learn about.

So it sounds like CRAB drugs don't really do much for remyelination... which is why the MRF is conducting its research on myelin repair treatments (doh!)

Another question, when someone gets to the point of SPMS are they usually taken off of CRABs? If so, what treatments are usually given at that point? Tysabri?

Ufrustrated -- If I see some of your neurons floating around (as I might go kayaking this weekend) should I ship them out to you? :)

[Ufrustrated2]

While you folks sort this out to better educate us, a quick note to Justine, if you see my neurons floating about in the Bay Area let me know. I think I lost about half of mine there. LOL

[jensequitur]

For shizzle... let's get Quizzle to weigh in on this topic!

[Lulu54]

hmmmmm.... why does this MiSerable disease so confound me and so many others?Like I said, I may have this all wrong and have already put in a house-call request to Q to see if she can set me straight.  :-)  

[jensequitur]

Not exactly...  As I understand it, a person with MS is losing neurons all the time.  During the early phases of the disease, the body has an immune response to the attack, and the brain becomes inflamed.  This is why they give you steroids for severe relapses - it allows the brain to not be quite so inflamed.

Now this is where I get confused!  I looked at an article on 'Neurogenesis and chronic lesions in multiple sclerosis' which is basically about how lesions in the brain of multiple sclerosis patients sometimes have more neurons than the surrounding tissue.  I think what they were trying to say is that the brain sometimes sends a signal to start growing more neurons in that damaged tissue.  And sometimes not.  The question is, what causes the brain to send the signal?  

It would be nice if the CRABs would encourage the brain to remyelinate.  Or if we could find a drug that would do that...  

[Lulu54]

I should have also written that the CRAB's are rarely used for SPMS  - they are mainly  first line treatments for MS. When you get to the point on chronicity with MS, you may very well not be on any of those DMD's.  

I hope some of this makes sense.
Lu

[Lulu54]

I may be totally wrong here, because I often am, but Jen may have used the wrong term here - when we are in relapse, I would think the myelin is being attacked.  It is when we are in the remitting  (remission) phase that our immune system quiets down and the body has a chance to send the linemen in and repair the faulty circuits.  

With RRMS we have periods of relapsing (attacks) and remitting  (disease withdraws) that plays havoc with our myelin.  When the RRMS changes, and becomes chronic the remitting goes away and we go into a more constant relapsing phase.  Often that RRMS converts to Secondard Progressive MS and RRMS is no more.

Now in my thinking, when we are on the DMD's the only thing we know for sure about them is they usually slow the number of relapse episodes down - giving our bodies more time to repair in between attacks.  

It would make sense in a connect-the-dots way then that DMD's would aid in the remyelination of the brain in a very round about way.  

Like Jen, I have not seen anything written on that one way of another though.

The article you referenced makes perfect sense - with milder forms of MS ( RRMS) the body has a chance to heal the lesions through remyelination.  With the chronic forms of MS, fewer of those lesions get healed.

I found the article very interesting - thanks for bringing it to our attention.

When Q comes back around I will ask her to check what I've written for accuracy ....

as always,
Lulu

[jensequitur]

Good question, don't know the answer.

What I do know is that lesions have an increased number of neurons, compared to the non-damaged areas.  Inflammatory disease activity destroys those neurons, and some are replaced by the body.  Studies suggest that the demyelinated white matter sends signals that either prevent or enhance the ability of neurons to regrow.

So it would logically follow that as the MS patient progresses, they stop having relapses.  If the relapse is sending a signal to the brain to regrow the neurons, without a relapse, there is no regrowth.

DMDs like avonex, betaseron, or rebif are supposed to slow down the relapse process - so it's possible that it would also slow down the remyelination.

But this is just theory!  I haven't seen ANYTHING that suggests that the DMDs slow down the remyelination of the brain.