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Thread: Who Plans to Attend Working 2 Walk 2011 ?

  1. #231
    I was just trying to follow your thought on the korean sci dogs citations.

  2. #232
    Only examples. The main work, as always, is made in rat models.
    -Ramps in buildings are necessary, but it would be usefull to have another ones for people (mind/heart).....

    -Hoc non pereo habebo fortior me

  3. #233
    jsilver, am I right drawing a conclusion that you don't have (even theoretically) any approach to try fixing harm, caused by TM?

  4. #234
    Good morning,

    TM; do you mean transverse myelitis? The issues regarding biologically based strategies to foster regeneration or sprouting following TM are likely similar to those following traumatic injury. However, it is conceivable that in either case, but possibly more likely after TM, that there may be many intact axons that have lost their myelin and have been made non-functional. Also, we are learning that there are many axons from various brainstem reticular (a more primitive system of circuits that support many basic functions) and propriospinal systems ( a multisegmental system of axons) that repeatedly cross the midline below the lesion. They can be a source for remyelination strategies as well as an anatomical source for sprouting strategies because they seem to have a strong potential to regenerate on their own. They just need help and in the respiratory system, chondroitinase is one way to wake them up. They can be re-awakened one full year after cord injury in rats. I will present this data at W2W. That's a very old rat and to my knowledge we are among just a minority of labs to have waited this long prior to therapy. Papers from the Mark Tuszynski, Wolfram Tetzlaff and John Houle labs also explored regeneration questions and strategies after a very long waiting periods with optimistic results. If one has a totally complete lesion we will have to find a way to bridge the gap and there are strategies to do this that can restore a good measure of function which I will discuss at W2W. Of course, there are other strategies using epidural stimulation and training plus circuit activating drugs that Reggie Edgerton and Susan Harkema are exploring as an alternative strategy. I would love to see our techniques dovetail with theirs and others who use FES approaches. As time passes beyond the initial lesion we will have to learn what hurdles develop that need to be overcome with good solid research. However, I will never tell you that we have all the answers today that will allow us to "cure" anybody with a chronic SCI within a relatively short time frame.

  5. #235
    Dr. Silver ,

    Hi, I am not sure if you explained this question in one of your posts or not (sorry if i missed it ,i could not find it or may be i did not understand ) : what is (are) exaclty and specifically stopping you from going to clinical trial right now with CHONDROITINASE ABC alone , or the combination of chondroitinase abc and nerve graft for chronic spinal cord injury in human? my understanding is that there are many published papers in addition to your work that suggest that this might works and might reverse paralysis (I think dr. young said in one of his posts that there are about 50 papers that suggest chondroitinase abc might helps in reversing paralysis due to spinal cord injury in rats at least to some extent ). thank you.
    Last edited by kz; 10-11-2011 at 10:22 AM.

  6. #236
    jsilver, thanks a lot for reply, but you have not mantioned the Adhesive process in the unfunctional part of spinal cord, that in case of TM is long-tracted and "bridging" technique won't help. You say that "there may be many intact axons that have lost their myelin and have been made non-functional", but after a long period of time (years) axons faded and need much more than only myelin for their revival. And if there is also massive damage to white and grey matter - only neurotransplantation with the complete set of helpers and supporters may (in theory) somehow lead to functional improvement. If I get you right, all that concerns to neurotransplantation, you may only speculate about. Would be glad to be wrong.

  7. #237
    Dear kz,

    The patent for chondroitinase use in SCI is held by Acorda Therapeutics so we are all waiting to hear what Tony Caggiano of Acorda is going to tell us at W2W. I and any others will keep showing good evidence of when and where the enzyme can work robustly but it will be up to the company to help with clinical trials. They have produced some top notch heat stable enzyme that a could help greatly. Since our Nature article came out a number of neurosurgeons have expressed interest in a potential clinical trial. I will be presenting a Grand Rounds in the early spring at UCLA to their neurosurgery department where there is a close friend of mine (and a world class neurosurgeon) who has expressed strong interest.

  8. #238
    Dear kivi66,

    I fully understand the issues involved with chronic injury and I appreciate your comments. I did mention the hurdles that need to be overcome in my post #234. However, just like after trauma both sensory and motor axons that were severed remain essentially indefinitely with dystrophic end balls at the outer edge of the penumbra of your lesion. Yes, we may need further strategies (likely neurotrophin support) to re-awaken these sleepy neurons or we may need to regulate the PTEN gene to strengthen their growth potential but they potentially could be triggered back to a growth mode. Whether they can reconnect with the neuropil beyond the lesion after many years is still unknown but we surely won't know unless we try and that is exactly what we wish to do. You don't need neurotransplantation, you need axonal regeneration, terminal arborization/sprouting near a potential target and synapse re-formation.

  9. #239
    Quote Originally Posted by jsilver View Post
    Dear kivi66,

    I fully understand the issues involved with chronic injury and I appreciate your comments. I did mention the hurdles that need to be overcome in my post #234. However, just like after trauma both sensory and motor axons that were severed remain essentially indefinitely with dystrophic end balls at the outer edge of the penumbra of your lesion. Yes, we may need further strategies (likely neurotrophin support) to re-awaken these sleepy neurons or we may need to regulate the PTEN gene to strengthen their growth potential but they potentially could be triggered back to a growth mode. Whether they can reconnect with the neuropil beyond the lesion after many years is still unknown but we surely won't know unless we try and that is exactly what we wish to do. You don't need neurotransplantation, you need axonal regeneration, terminal arborization/sprouting near a potential target and synapse re-formation.
    Jerry,

    Thank you for joining this forum and sharing your expertise and opinions.

  10. #240
    Senior Member lynnifer's Avatar
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    Quote Originally Posted by quadfather View Post
    Jerry,

    Thank you for joining this forum and sharing your expertise and opinions.
    x2 I have Transverse Myelitis. I would give anything to pee normally again! lol I'm about to look into an artificial sphincter ... I wish this research was 10yrs further down the road for me.
    Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

    T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

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