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Thread: Stephen Davies Update

  1. #391
    Banned adi chicago's Avatar
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    Great news Dr.Davies ....Thank you very much for your hard work.
    • Dum spiro, spero.
      • Translation: "As long as I breathe, I hope."

  2. #392
    Senior Member redbandit's Avatar
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    I am on the J. Biol e-mail list and have been anxiously awaiting to see this paper! Thank you Dr. Davies, your lab and your collaborators for your dedication to a challenging biological puzzle!

  3. #393
    2-3 Years for clinical trial, sounds awesome. I realise this is if everything goes well, but its definitely something to look forward to!!

    Thanks again for all your (and your teams) work Dr. Davies!

  4. #394
    O.k., I've read all the information posted and I haven't seen the word chronics in there once. Is this breakthrough only for acute injuries, or do chronics apply as well? When I read about the breakthrough I almost fell out of my chair I was so excited, but the more I read the more the excited feeling left my body. Don't get me wrong, I'm happy either way but lets face the truth, we all want to walk again. Whats with the decorin research, does it work on chronic injuries? Does the new breakthrough work on severed, and chronics as well as acutes? I need to know because I'm still curious how to go about being part of the clinical trials. I read if all goes well the clinical trials should be started in 2-3 years. Which leads me back to my question, does this apply to chronics and severed cords? An answer would be more than appreciated. Thank you.

  5. #395
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    Quote Originally Posted by Han Solo
    O.k., I've read all the information posted and I haven't seen the word chronics in there once. Is this breakthrough only for acute injuries, or do chronics apply as well? When I read about the breakthrough I almost fell out of my chair I was so excited, but the more I read the more the excited feeling left my body. Don't get me wrong, I'm happy either way but lets face the truth, we all want to walk again. Whats with the decorin research, does it work on chronic injuries? Does the new breakthrough work on severed, and chronics as well as acutes? I need to know because I'm still curious how to go about being part of the clinical trials. I read if all goes well the clinical trials should be started in 2-3 years. Which leads me back to my question, does this apply to chronics and severed cords? An answer would be more than appreciated. Thank you.
    Very good question han solo.I hope that we will get an answer regarding acutes and chronics .
    • Dum spiro, spero.
      • Translation: "As long as I breathe, I hope."

  6. #396
    Hi Everyone,
    Here is the link to the full version of the paper. http://jbiol.com/content/pdf/jbiol85.pdf

    This study have several important findings that are applicable to cell based therapies for both acute and chronic SCI.

    Controlling what stem cells turn into is vitally important.
    One of the most important findings of our paper is that it clearly shows that not all cells that can be made by embryo-derived stem cell like cells are necessarily benefial for SCI repair. Controlling the differentiation of stem cells (what they turn into) before transplanting them into the injured spinal cord (at any stage after injury) is essential for promoting repair and - avoiding severe side effects such as neuropathic pain (allodynia).

    In 2005 the Olson researrch group in Sweden published a really important paper in the journal Nature Neuroscience that showed that if you transplant "naive" stem cells into the injured spinal cord, they turn into astrocytes and induce severe neuropathic pain (technical term is allodynia). This created a real worry for those of us who were trying to make astrocytes to repair the spinal cord.

    However what we have found is that it is a sub type of astrocyte - the GDAsCNTF - that can be made from stem cell like cells - the GRP cells - that give no recovery and promote severe allodynia (both mechanical and thermal sensitivity). When we transplanted naive GRP cells into spinal cord injuries we also saw that they turned into astrocytes and failed to promote recovery but did induce severe allodynia.

    Importantly, when we tested spinal cord inured animals that had received GDAsBMP there was no allodynia (mechanical or thermal).

    There has been an old idea that any therapy that promotes nerve regeneration will also cause unwanted sprouting of pain circuits (c-fibers that contain a peptide called CGRP, see figure 11 in the paper). However what we found was that the GDAsBMP promote regeneration of nerve fibers - without promoting unwanted sprouting of pain circuits (see fig. 11 of the paper). Thus GDAsBMP give all the "gains without the pain". Naive stem cells, GRP cells or the astrocytes such as GDAsCNTF that they can make, however give no gains and a lot of pain.

    DO NOT LET ANYONE INJECT NAIVE "STEM CELLS" OF ANY KIND INTO YOUR SPINAL CORD, EITHER IN ACUTE OR CHRONICALLY INJURED CORD !!

    Do not let anyone inject astrocytes into your cord that have been made made by giving CNTF to stem or precursor cell cultures (some research groups are proposing this).

    My co-authors and I strongly suggest that all potential cell based therapies for SCI must be rigorously tested for severe side effects such as allodynia before going to clinical trails in humans.

    Note that many stem cell based / SCI studies (e.g. many of those at Geron) have been conducted in "nude" rats and mice that have impaired immune systems so they won't reject transplants. Nude rats and mice do not develop neuropathic pain after SCI or peripheral nerve damage.

    Making the right kinds of spinal cord cells for spinal repair.
    Our new paper confirms that GDAsBMP are an optimal type of spinal cord cell for repairing spinal cord injuries. So far we have peer reviewed data showing 27 out of 27 rats that have received these cells have achieved robust improvements in cordinated limb movement (and many more examples in the lab at the moment). In addition to being able to form bridges for regenerating nerve fibers, the GDAsBMP are able to protect injured neurons from undergoing atrophy (the stem cell like GRP cells and the other kinds of astrocytes the GDAsCNTF both failed to do this).

    Are all immature astrocytes the same?
    Astrocytes account for roughly 70% of cells in the adult human central nervous system, however remarkably little is known about different types of astrocytes or their functions. What is known is that the embryonic spinal cord does not form scar tissue, allows nerve regeneration and recovery of function and does not develop neuropathic pain after injury.

    There has therefore been a long standing interest in transplanting immature astrocytes into the injured adult cord, however the results were dissapointing in early experiments in the 1980's and early 1990's and we think this was due to the fact that the transplants contained mixed types of astrocytes and were contaiminated with naive precursor cells and inflammatory cells (microglia). It also took a month or more in to make these early tissue cultures of presumably mixed types of astrocytes and it has been shown that with prolonged time in culture, these astrocyte cultures also lost what ability they had to support growth of nerve fibers.


    What we have discovered is that by using GDA technology we can rapidly generate highly purified, large populations of specific and desirable astrocytes like the GDAsBMP (within a week) and avoid making highly undesirable astrocytes like GDAsCNTF or contamination with naive stem cells / precursors that give no recovery and instead promote severe pain.

    Neuropathic pain
    Adult astrocytes are known to form CNS scar tissue and it is thought that many of the astrocytes within spinal cord scar tissue are generated from adult stem cell like precursor cells already in the adult spinal cord. When we looked in normal untreated spinal cord injuries we found a sub-type of adult astrocytes (see Fig 3 panel c in the paper) that have many of the characteristics of the GDAsCNTF that promote pain syndromes. As we know what inflammatory signal molecules such as CNTF (which is found within adult injured cords) can turn glial precursors into highly undesirable astrocytes like GDAsCNTF that promote pain, this paves the way to developing new therapies for blocking the generation of such "bad astrocytes" and induction of pain syndromes.

    Normally astrocytes have a finite lifespan and are replaced. Theoretically therefore it may be possible to gradually lower the numbers of adult GDAsCNTF-like astrocytes in chronically injured cords which may result in a reduction of neuropathic pain. This is just a theory at the moment but one we can test.

    Chronic SCI
    Quite rightly most people on this forum want to know about GDAs and treating chronic SCI. Yes the new paper has only looked in acute SCIs, however we now know which types of astrocytes to make and ones to avoid when turning our attention to Chronic SCI.

    Other groups have shown that even mixed populations of immature astrocytes are very good at making neurons make new connections in tissue culture. Based on this data we feel it is highly likely that GDAsBMP are very good at doing the same and this may in part account for why we see such robust recovery in animals that are treated with these cells. Plasticity (the ability of surviving nerve fibers to make new connections) is thought to play a major role in recovery from SCI. We are hoping therefore that GDAsBMP will be able to promote plasticity and the formation of new connections (called synapses) when transplnated into chronically injured spinal cords.

    My lab is committed to developing new therapies for chronic SCI. We have developed new tests for showing recovery in chronic SCI rats (because their weren't any reliable ones). We have developed a new infusion system suitable for treating chronic SCIs with decorin (because there wasn't one available). The lab has switched its main emphasis to chronic SCI. By their very nature chronic SCI experiments take a lot longer to conduct. Experiments are underway in the lab and we will publish the data as soon as the experiments are completed and properly documented.

  7. #397
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    Chronic SCI
    Quite rightly most people on this forum want to know about GDAs and treating chronic SCI. Yes the new paper has only looked in acute SCIs, however we now know which types of astrocytes to make and ones to avoid when turning our attention to Chronic SCI.

    Other groups have shown that even mixed populations of immature astrocytes are very good at making neurons make new connections in tissue culture. Based on this data we feel it is highly likely that GDAsBMP are very good at doing the same and this may in part account for why we see such robust recovery in animals that are treated with these cells. Plasticity (the ability of surviving nerve fibers to make new connections) is thought to play a major role in recovery from SCI. We are hoping therefore that GDAsBMP will be able to promote plasticity and the formation of new connections (called synapses) when transplnated into chronically injured spinal cords.

    My lab is committed to developing new therapies for chronic SCI. We have developed new tests for showing recovery in chronic SCI rats (because their weren't any reliable ones). We have developed a new infusion system suitable for treating chronic SCIs with decorin (because there wasn't one available). The lab has switched its main emphasis to chronic SCI. By their very nature chronic SCI experiments take a lot longer to conduct. Experiments are underway in the lab and we will publish the data as soon as the experiments are completed and properly documented.
    [/quote]
    Thank you for the info Dr.Davies.........I see a cure for all sci in sight soon.
    God Bless....
    • Dum spiro, spero.
      • Translation: "As long as I breathe, I hope."

  8. #398
    Senior Member Jeff B's Avatar
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    Thank you Dr. Davies for your commitment and contribution to SCI repair and for keeping us in the loop.

  9. #399
    Nice to see some faces above the tall overgrowth that has come to characterize the field of PROGRESSIVE spinal cord injury research. Thank you Sir.

    f
    ight

  10. #400
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    Davies. Great going further on for this quest, and as you wrote Lars Olson studies from Karolinska research helped which by you’re study seems to be valid, but the Karolinska Nobel institute bunch should look at studies like yours to move basic research to the clinics, but are they, really? I do not think so, they get millions after millions, and research and research, -I say give money on focused research, and as for SCI research I think this is valid, these days. Like you’re study might show one can focus on SCI and not solely focus on basic research in general. So thanks for that.

    Other groups have shown that even mixed populations of immature astrocytes are very good at making neurons make new connections in tissue culture. Based on this data we feel it is highly likely that GDAsBMP are very good at doing the same and this may in part account for why we see such robust recovery in animals that are treated with these cells. Plasticity (the ability of surviving nerve fibers to make new connections) is thought to play a major role in recovery from SCI. We are hoping therefore that GDAsBMP will be able to promote plasticity and the formation of new connections (called synapses) when transplnated into chronically injured spinal cords.

    Isn’t plasticity known as for example like brain strokes for the different synapses connections and grids to learn new usage, meaning already some existing neuronal grids exists, by making detours or otherwise, by some existing networks, to make connections (obviously like in the real injured cord does not happen)? And if not existing neighbouring connections in the cord to help out, how does one create a good neuronal grid at the injury site and other lost dead long wire connections in the chronic injured cord to send ascending and descending signals communicating signals in this grid to restore it, when the rest of the even close grid in the cord are destroyed, like for example long axons controlling motomovement say in legs in the human body to reconnect when controlling neurons in the grey matter is destroyed? How will one go by such scientific quests to overcome such hurdles, growing back long paths of axons in the human body, and replacing neuronal motoneuronal cells, -what could a scientific strategy be as for this? Difficult questions, still.

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