Research Day Talk Genetics

Today, Ram winds up the session on UCLP science with a talk on the genetics of MS.

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  • As I was looking at the vid a question came into my mind.

    If we assume that evolution is a not stopping ongoing process, could it be that MS is an odd outcome of a "failed" evolutionary process?

    • Oh please, the last thing MSers need is being stigmatised as biologically disfunctional 'not-quite-evolved' ergo degenerate humans. It's an illness which is complex but I would not search inside the body of MSers for an explanation why the cause has not been found yet. More likely that resources are put to causes which are more popular.

  • Armchair scientist here, so maybe Ram will correct me if I'm wrong, but …

    I don't think our MS genes reflect a failing evolutionary process. Genes mutate. Sometimes those mutations are passed on and sometimes they're not. The way a mutation fails to be passed on is by causing early death (via miscarriage or childhood disease in the carrier) or by causing its carrier to not reproduce (that is, people that carry the gene aren't fertile or are unlikely reproductive partners). Since most people who carry MS genes don't get MS, the likelihood of an MS gene being bred out of the human genome is pretty slim.

    All of us come into this world with about 60 new mutations (out of 3.1 billion AT/GC pairs). More if your father was older when you were conceived.

    The fact that MS is becoming more prevalent, not less, tells me that the genes that cause it are doing quite well. No evolutionary failing here!

    • I don't mark "failed" with being wrong or bad or whatever moral category you like to mark it. Nature doesn't work this way.

      I'd like to see a comparison between the genetic sequence of a person of lets say 3000 years ago, MS'ers and "normal" ppl.

      Just purly out of academic interest. E.g. if MS genes become more prevalent, does it mean, that there is a evolutionary process going on?

      I don't see all symptoms of MS as negativ. Some also have quite good aspects.

      P.S.: I have MS.

    • Nah, I didn't think you were placing a value judgment on our gene. When you think about it, if we all have the HLA-whatever gene, we probably all have a common ancestor and then we're all kin here, aren't we? 🙂

      I was mostly spouting off because I took a class in genetics and evolution recently and it's now one of my favorite topics. Are you thinking that the gene might be increasing its presence in the human population over time because it provides some reproductive/survival advantage in ways we haven't even thought of–perhaps less cancer to those of us with hyper-vigilant immune systems? That would be interesting to know.

    • "Are you thinking that the gene might be increasing its presence in the human population over time because it provides some reproductive/survival advantage…"

      Sort of.
      E.g. I have sensing problems with temperature. So I don't feel cold tempersture as fast as most ppl. And I don't mean the average male /female sensing of tempersture.
      It's the same with heat. I can take caseroles out of the oven without protection and don't get burn marks (within a specific time).

      Just as an example.

      Yes, could also be a cancer thing. Which I think has already been studied and no evidence has shown up.

      I wonder if we could see any relevant differences of genetic sequences in a person of 3000 or maybe 5000 years ago (if this is possible at all) and todays ppl and MS'ers.

      Wouldn't it be interesting? Even if it wont show differnces in the specific sequences.

    • Geneticists know interesting things about the gene for lactase tolerance. That is, it's a relatively recent mutation that makes some people able to digest lactase comfortably after early childhood. I don't know how they figured out when the gene was introduced (probably something to do with comparing gene sequences and then doing a bunch of math). If Ram ever reads this thread, maybe he can explain whether the mutations that lead to MS-friendly genes are fairly recent, have been there since we were slime in a warm pool somewhere, or not ever investigated.

  • Hi Cat and Marc, interesting discussions you are having! I will give you my two pence worth.
    The main gene for MS- called HLA-DRB1- comes in many forms. A certain form called 15 increases the risk of MS. The available genetic data so far are largely consistent with a model where different forms of this gene have evolved independently for tens of millions of years. DRB1-15 is much more common in Europe (or European derived populations e.g. Canada and Australia) than in Asia. Current thinking is that the increased frequency of DRB1-15 in Europe was because of a survival advantage that having this allele conferred in this region- most likely protection against a pathogen of some sort. It is thought that DRB1-15 would have been extremely good at eliciting an immune response against this pathogen (that may or may not exist any more) but with additional exposures this may lead to MS developing in some people…
    Hope that makes sense!

    • Hi Ram,

      thanks for this short and interesting explanation.
      Do you also have knowledge on how this gene evolved or differentiates in more hetereogenous regions like e.g. Southern America where native ppl and European colonists "mixed" up more over the years than e.g. Northern America / Canada?

      This could also be an explanation why NMO is more common in Asia than MS, as asian society is more homogenous. So IF this would be correct assumption science should notice an increase in MS within lets say 100-200 years in the asian society as the society gets "more" european.

  • Thanks a million Ram! Fascinating information.

    That makes a lot of sense that DRB1-15 might have been advantageous against a pathogen at one time in light of the fact that it's on a known part of the gene that influences the immune system. Makes me wonder if this pathogen looked something like a variation of modern HERV or EBV.

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