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Li & Strittmatter (2003). Delayed systemic nogo-66 receptor antagonist promotes recovery from spinal cord injury.

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  • Li & Strittmatter (2003). Delayed systemic nogo-66 receptor antagonist promotes recovery from spinal cord injury.

    • Li S and Strittmatter SM (2003). Delayed systemic nogo-66 receptor antagonist promotes recovery from spinal cord injury. J Neurosci 23:4219-27. Summary: Traumatized axons possess an extremely limited ability to regenerate within the adult mammalian CNS. The myelin-derived axon outgrowth inhibitors Nogo, oligodendrocyte-myelin glycoprotein, and myelin-associated glycoprotein, all bind to an axonal Nogo-66 receptor (NgR) and at least partially account for this lack of CNS repair. Although the intrathecal application of an NgR competitive antagonist at the time of spinal cord hemisection induces significant regeneration of corticospinal axons, such immediate local therapy may not be as clinically feasible for cases of spinal cord injury. Here, we consider whether this approach can be adapted to systemic therapy in a postinjury therapeutic time window. Subcutaneous treatment with the NgR antagonist peptide NEP1-40 (Nogo extracellular peptide, residues 1-40) results in extensive growth of corticospinal axons, sprouting of serotonergic fibers, upregulation of axonal growth protein SPRR1A (small proline-rich repeat protein 1A), and synapse re-formation. Locomotor recovery after thoracic spinal cord injury is enhanced. Furthermore, delaying the initiation of systemic NEP1-40 administration for up to 1 week after cord lesions does not limit the degree of axon sprouting and functional recovery. This indicates that the regenerative capacity of transected corticospinal tract axons persists for weeks after injury. Systemic Nogo-66 receptor antagonists have therapeutic potential for subacute CNS axonal injuries such as spinal cord trauma. Department of Neurology and Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520.

  • #2
    Interesting. Is this study ongoing or are they offering this to newer injuries yet? Will they?


    • #3
      This is in rats... Biogen is developing this for clinical trial and I am quite excited about the this therapy.


      • #4
        "partially account for this lack of CNS repair"

        For me the question still being, is it actually a lack, or is it parts of the repair procedures.

        If there are damaged cells in alike an inter-highway of up & down connections, among the last thingies they might need is being disturbed in their repairs
        by loads of other stuff transpassing the sector.

        The demylination might prevent being alike overrun by signals, for which the sector is no longer in a status for.

        So it might have an important natural function.

        Before being sure it has not, my question remains if it does not have this function also.


        • #5
          How was the rats recovery of axons monitored?
          Would this be a one time usage? Are the folks
          at Yale saying it can be administered subcutaneously? This really is exciting.
          Does Biogen want some canines to test it on?
          Sorry, always looking out for our downed babies.
          Life isn't about getting thru the storm but learning to dance in the rain.