Guest Post- Animal Studies Enough Already

In response to Yesterday’s Post

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Enough with the mouse studies, already! In the 15 years since my diagnosis, I’ve read countless research reports involving EAE and other mouse models of multiple sclerosis. Only an infinitesimal amount of these reports have ever proven to have any real relevance to the human MS population.

The simple fact is this: mice don’t get ms. You can inject them with myelin or other toxins and achieve something that kind of sort of looks like MS, but it’s not ms. Then, it seems as if staring intently at the mice long enough or breathing on them shows some kind of benefit. Honestly, it’s almost come to that level of ridiculousness.

We must come up with better models of the disease to work on. The amount of time and money wasted on mouse studies is – given the the enormity of the impact of MS on those humans it attacks – obscene.

Really, it’s time to rethink our entire approach to MS research. Thus far the best we’ve come up with are treatments that profoundly suppress parts of the intricate human immune system, the long-term effects of which are a complete unknown. And these treatments do absolutely nothing towards effecting a cure.

Given modern laboratory techniques, the rapid advances in computational power, the emergence of AI, and the vast body of knowledge accumulated by ms researchers and clinicians, one would think a coordinated, concerted effort to finally identify the cause or causes of the disease might finally bear fruit. Time spent fixated on mice with induced conditions that sort of resemble MS is, at this point, time wasted. And those of us forced to watch ourselves disappear by inches don’t have that time to waste.

Patients should be rising up against the status quo, but unfortunately most are too busy just trying to get through the day with some modicum of functionality and dignity left intact. MS has gone from medical backwater to one of the most profitable areas of medical practice in the last two decades. It’s high time to cure the damn thing and send it back from whence it came. We now have the technology and basic understandings of the mechanisms to get this done, given the will. Coming up with an effective anti-EBV treatment would be a great first step…”

This was a comment made yesterday and is an opinion I am sure many people hold. Likewise, many neuros think the same.  However, basic science is the basis of where treatments come from. 
I was at a recent meeting about finding treatments, which may involve a bit of screening in animals and a very eminent scientist said (Paraphrased) I’m not going to do that as I’m not interested. All I am interested in doing is looking at mechanisms of biology. 

However they are very happy to take money from disease-related charities.

What you do think?

The science publishing system has created a “mechanism is all mentaility” and disease can simply be a vehicle to get research support. 

However times are changing and it is increasingly difficult to get funding for animal studies. However, without knowledge, we will continue to shoot in the dark.

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  • Wow! Wasn't expecting this to be used as a guest post, but I guess I'm flattered.

    I only wish I had known it would be used as such, because I would have cleaned up the grammar a bit and attempted to make the prose a bit more elegant.

    I apologize in advance for my one grumpiness. It's just that I've been at this for 15 years, watching myself steadily disappear and have had more than my fill of research report after research report involving mice amounting to just about nothing.

    Thanks for featuring my comment, I hold your group in very high esteem and I hope my words aren't seen as disparaging your work.

    • Sorry I should have written to you, but your comment makes a point and it is something we have to grapple with.

      I believe animal work has its part to play, but doing animal work for the sake of doing animal work should of had its day. However it hasn't and there are many esoteric animal studies reported that you have to ask should we be doing these studies. Most of them never get reported on here, as I get enough abuse without adding more from my peers:-(

      For some the answer is yes, others maybe, but there is a far amount of no..don't do it. This is of course my opinion….Maybe I am being grumpy.

    • TWK it's a great comment and your frustration is justified. I am grateful to the mice for leading researchers towards immunosuppressants and the first dmts. I trust the Barts MDs completely but dread to think about unnecessaary and pointless experiments in less-regulated countries. The BartsMS team have published some stunning papers recently by reading and without going near a lab. Particularly love the FoI requests – all that data out there!

  • Anything shown in mice has to be presented with the caveat that the findings apply to mice and not (necessarily) humans, right? Leave the rodents alone, I'd say.

    Anyway, that simple antivirals have not yet – to my knowledge – been properly trialled for MS is nothing short of an absolute travesty.

  • Herpes viruses are part of a subfamily of the virus called alphaherpesvirinae, which is known to infect and then hide in nerve cells. The immune system has learned to treat these viruses with "kid gloves", because immune cells can't outright kill these herpes viruses without killing the nerve cells that serve as a host.

    It is known, that tranylcypromine can keep herpes viruses in latent mode by inhibiting LSD1.

    Many researchers suspect that HHV-6A actives latent EBV in B-cells resident in MS lesions.

    Couple decades were not enough to raise money for good viral-targeted research?
    How long we will call MS "autoimmune disease"?


    • Yes, where is the purported auto-ag(s) after all these years? I agree that anti-virals need to be looked into but the current consensus of targeting peripheral lymphocytes seems to be accepted as the be all end all. The mouse model does not represent the origin of the CNS inflammation and therefore is limiting.

  • I wholeheartedly agree with what Mark says. I feel I have been so sucked in – as has my MS researcher daughter. She did her PhD on finding a better mouse model (louse model?) and she actually had a desk next to a student who gathered the data that identified the MS propensity genes.
    One question. I can see the strength of this argument regarding Phase 3 trials. Is it as strong for Phases 1 and 2?

  • Well said everyone! Few would dispute that there is no naturally occurring or experimentally produced CNS disease that convincingly resembles MS, mores the pity. Few would dispute that MS is clinically, pathologically, epidemiologically and immunologically highly distinctive, we can say, unique to homo sapiens. This implies a highly distinctive pathogenesis.
    Gay has produced evidence that this is primarily anatomical. Have a look at Gay F MSARD 2013 2,213, and then reflect on in-out-in!

  • Prof Hauser in this video mentions that they were searching for an animal model with more fidelity and they had finally found it, in…1988. What happened to that?

    (at 21.0)

    Also, why the thing works with theory first, experiment later and not the opposite? Why does it take so damn long to try existing drugs? If we would get to try all drug compounds we have -even blindly, even in the mouse model-, and then try to understand why those that worked worked, we would save time and lives.

  • The problem is that the people who have made their career on the EAE model are the ones who sit on the study sections/grant review committee. I submitted a grant to study the interaction between EBV and MS in our mouse model, but it didn't get funded because–according to them–the relationship between EBV and MS wasn't well established. So we are left with the same old models that don't work very well.

  • Seems like many of us humans with MS (especially progressive MS) would be willing to volunteer for clinical trials. I've long felt we were all in some huge experimental trial anyway. Millions of us take DMT's which don't do much to slow progression or prevent transition to SPMS. Lesion load and active lesions are the hallmark of success or failure of a particular drug but lesion load isn't really correlated to functionality and loss of gray matter isn't even tracked. Sometimes I think We should be paid to take these crappy drugs.

    • True, these DMTs will not prevent progression eventually taking hold. It is a moneymaking jolly.

  • Brilliant Guesspost! We all hold researchers dear to our hearts and hold them in high esteem but we also become very, very frustrated through fighting a losing battle – so it's SO good to hear someone pop the cork. I heard this week that they are about to find a cure for the common cold – is that good or bad news for a cure for MS?! Lets pull the anti-virals out of the hat! But don't give them to Mickey or Minnie, please.



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