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Thread: Spinal Cord Injury Network USA (SCINetUSA)

  1. #301
    Quote Originally Posted by keeping on View Post
    Dr Young, I understand that Dr D. Kerr is leaving Johns Hopkins and going to Boston. Is this a discouragement to the cause or is it something positive? I was inquiring about a 2006 article that was published where he had success with stem cell with rats. I know you have mentioned him several times. I would like to know what the stauts of his research is at this time.

    Thanks in advance,
    I don't know enough about what will happen to comment. Of course, if Dr. Kerr leaves Johns Hopkins, this will be a blow to Johns Hopkins and the very important transverse myelitis clinic that he has there. On the other hand, I am confident that he will do good wherever he goes because I believe that his goal to help achieve the cure for people with transverse myelitis and spinal cord injury. Wise.

  2. #302
    Thank you Wise. I just wonder what will happen with the transverse myelitis program and research at Johns Hopkins?

    Thank you Wise

  3. #303
    Wise, what about the article I mentioned and the progress, if any, since?

    Thanks in advance

  4. #304

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    Wise here is article from Johns Hopkins for study on embryonic stem cell on rat from 2006


    Hopkins Scientists Use Embryonic Stem Cells, New Cue to Awaken Latent Motor Nerve Repair

    If you have questions about this research, please call 410.614.6651
    June 20, 2006 -- In a dramatic display of stem cells’ potential for healing, a team of Johns Hopkins scientists reports that they’ve engineered new, completed, fully-working motor neuron circuits -- neurons stretching from spinal cord to target muscles -- in paralyzed adult animals.
    The research, in which mouse embryonic stem (ES) cells were injected into rats whose virus-damaged spinal cords model nerve disease, shows that such cells can be made to re-trace complex pathways of nerve development long shut off in adult mammals, the researchers say.
    “This is proof of the principle that we can recapture what happens in early stages of motor neuron development and use that to repair damaged nervous systems,” says Douglas Kerr, M.D., Ph.D., a neurologist who led the Hopkins team.
    “It’s a remarkable advance that can help us understand how stem cells can begin to fulfill their great promise,” says Elias A. Zerhouni, director of the National Institutes of Health. “Demonstrating restoration of function is an important step forward, though we still have a great distance to go.”
    The researchers created what amounts to a cookbook recipe to restore lost nerve function, Kerr explains. The approach could one day repair damage from such diseases as ALS (Lou Gehrig’s disease), multiple sclerosis or transverse myelitis or from traumatic spinal cord injury, the researchers say. “With small adjustments keyed to differences in nervous system targets,” Kerr says, “the approach may also apply to patients with Parkinson's or Huntington’s disease.”
    In a report on the study, to be released online June 26 in the Annals of Neurology, the Hopkins team says 11 of the 15 treated rats gained significant, though partial, recovery from paralysis after losing motor neurons to an aggressive infection with Sindbis virus -- one that, in rodents, specifically targets motor neurons and kills them. The animals recovered enough muscle strength to bear weight and step with the previously paralyzed hind leg.
    Kerr likens the approach to electrical repair. “Paralysis is like turning on a light switch and the light doesn’t go on. The connectivity is messed up but you don’t know where. We’ve asked stem cells to go where needed to fix the circuit.”
    For a brief period after a nerve dies, it leaves behind what’s essentially an empty shell, with some scaffolding and non-nerve substances remaining. But with ES injections at the right time and place, and by adding the right cues, we’ve learned to restore the biological ‘memory’ for growing neurons, which is clearly still in place,” he added.
    The motor circuit engineering combines recent discoveries on stem cell differentiation, a growing understanding of early development of the nervous system, and insights into behavior of the nervous system in traumatic injury, Kerr notes.
    “As adults, our cells no longer respond to early developmental cues because those cues are usually gone,” says Kerr. “That’s why we don’t recover well from severe injuries. But that’s what we believe we have changed. We asked what was there when motor neurons were born, and specifically what let motor neurons extend outward. Then we tried to bring that environment back, in the presence of adaptable, receptive stem cells.”
    In the study, Kerr’s team first pre-treated cultures of mouse embryonic stem cells with growth factors that both increase survival and prompt specialization into motor neurons. Adding retinoic acid and sonic hedgehog protein -- agents that direct cells in the first weeks of life to assume the proper places in the spinal cord -- readied the conditioned ES cells for the motor neuron circuit that starts in the spinal cord. Then, stem cells were fed into the paralyzed rats’ spinal cords.
    Extending new motor neurons in an adult nervous system, however, meant overcoming hurdles. One involved myelin, the fatty material that insulates mature motor neurons. Like the coating on electrical wire, myelin prevents weakening of the traveling electrical impulse and lets it continue long distances. In humans, the myelinated sciatic nerve, for example, exits the spinal cord and extends to the leg muscles it activates, carrying impulses several feet.
    Once laid down, however, myelin inhibits further nerve growth -- nature’s way to discourage excessive wiring in the nervous system. “We had to overcome inhibition from myelin lingering in the dead nerve pathways,” Kerr explains. Two recently-developed agents, rolipram and dbcAMP enabled that.
    The assorted treatments let the new motor neurons survive, grow through the spinal cord and extend slightly into the outlying nervous system. A second hurdle remained in getting the neurons to skeletal muscle targets.
    As suggested by earlier work by team member Ahmet Hoke on repair in the outlying, peripheral nervous system, the researchers applied GDNF, a powerful stimulator of neuron growth, to the remains of the newly-dead sciatic nerve at a point near its former leg muscle contacts. GDNF attracted the extending motor neurons, “luring” them to the muscles. To ensure a continuous supply of GDNF, the researchers relied on injected fetal mouse neural stem cells, a known source of the molecule.

    Of some 4,100 new motor neurons created in the spinal cord, roughly 200 exited the cord and 120 reached skeletal muscle, forming typical nerve-muscle junctions, with appropriate, typical chemical markers. Microscopically, the neurons and their muscle associations appear identical to natural ones in healthy animals.
    Fifty of the new neurons were found to carry electrical impulses. (Because such testing is time and labor intensive, only a small area of leg muscle was assayed. The improved ability of treated rats, however, suggests more functional neurons are likely.) The rats gained weight, were more mobile in their cages and measures of muscle strength increased.

    Animals treated without even one component of the “cocktail” experienced no such recovery. Novel ways of tracing the neurons back to their source assured the scientists that they indeed had come from the injected stem cells, not from lingering host neurons.

    Research begins this summer to see how well the technique applies to human nerve recovery, using federally-approved human ES cells in larger mammals like pigs, Kerr says. Each of six academic institutions in a new collaboration will tackle a different major question of safety and effectiveness. Questions of tumor-formation, often a concern with ES cells, of the safety of surgery and of the ES cells’ ability to form healthy motor circuits are major questions to answer. Several years of testing and thorough data evaluation would occur before applying to the FDA to approve human clinical trials. The study was supported by Families of SMA, Andrew’s Buddies/Fight SMA, the ALS Association and The Robert Packard Center for ALS Research at Johns Hopkins, the Muscular Dystrophy Association, Wings Over Wall Street, and a grant from the NIH.

    Kerr is a grantee of The Packard Center for ALS Research at Johns Hopkins. He also directs Project RESTORE, a Hopkins-based undertaking to advance therapies for transverse myelitis and multiple sclerosis.
    Others on the research team from the Department of Neurology at the Johns Hopkins University School of Medicine include Jeffrey Rothstein, M.D., Ph.D.; Ahmet Hoke, M.D., Ph.D.; Nicholas Maragakis, M.D.; Yun Sook Kim, Ph.D.; Sonny Dike, M.D.; Deepa Deshpande, M.S.; Chitra Krishnan, M.S., and Jennifer Drummond. Researchers from the Department of Molecular Microbiology and Immunology at the Johns Hopkins University Bloomberg School of Public Health include Jessica Carmen, Tara Martinez and Irina Shats. Jeremy Shefner, M.D., Ph.D., of the Department of Neurology at the State University of New York Upstate Medical University, Syracuse, N.Y., also contributed to the study.

  5. #305
    Dr young, what do you think of the post I made as to research by researches at Johns Hopkins? The report is in the above post.

    thanks in advance

  6. #306
    Dr Young, please reply.


  7. #307

    What did you say Wise?

    Wise,we discussed Dr Kerr leaving Johns Hopkins and going to Boston. You mentioned an endeavor he is pusing for transverse myelits. What was it you said he is contemplating? I can't find it anywhere.

    Thanks in advance

  8. #308
    Wise, please respond; where is Dr Kerr going, and what are his plans for transverse myelitis.
    Thanks in advance,

  9. #309
    Keeping On, can you read?

    Quote Originally Posted by Wise Young View Post
    I don't know enough about what will happen to comment

  10. #310
    Dr Young, I'm seeing alot of recent pulications siting large advances of stem cells over the last 15 years. This is very disconcerting to us that are lloking for some sort of REAL therapy in the near future.

    When can we as victims of these horrible coinditions see some real human trials : not for eyes or hearts, but for spianl cord problems. Not for rats. or other animals but for HUMANS.

    Thanks in advance

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