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Mice movement neurons regenerated after spinal cord injury

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neuronResearchers have been searching for decades for a way to mend damage to the spinal cord, an injury that can lead to life-long paralysis. Even the smallest of breaks in these crucial central nerve fibers can result in the loss of leg, arm and other bodily functions. And attempts to prompt healing, through stem cells or growth factors, have yet to achieve widespread success.

Previous research had been stepping closer to encouraging neuronal growth—which usually stops after physical maturation. And a 2008 study co-authored by Zhigang He, a neurologist at Children’s Hospital Boston, announced success in shutting down a gene that stops neuron cell growth, thus enticing damaged nerves to start growing again. Through that process, the team was able to reestablish a severed optical nerve connection in mice. 

A new study, co-authored in part by He and other members of the 2008 team, demonstrates nerves necessary for voluntary movement could be regenerated in mice with spinal cord damage after removing a common enzyme that regulates the neuronal cell growth.* The results were published online August 8 in Nature Neuroscience (Scientific American is part of Nature Publishing Group).

The removed enzyme PTEN, a phosphatase and tensin homolog, helps to dictate activity in the mTOR pathway, which plays a role in cell growth. During maturation, PTEN is activated, halting cell regeneration, but after removing it from a group of experimental mice with spinal cord injury, the neurons grew as they did in the development phase.

The researchers propose that "neuronal growth competence is dependent on the capability of new protein synthesis, which provides building blocks for axonal regrowth." Restarting the mTOR pathway, what the authors term a "’rejuvenation’ strategy," could "be widely applicable for promoting successful regeneration following many types of injuries or traumas in the adult [central nervous system]."

Reestablishing this communication across those broken synapses could be life-changing for the millions of people who live with spinal cord injury across the world—especially given that the majority of cases occur in middle age, when these neuron cell growth pathways are already shut down. "Paralysis and loss of function from spinal cord injury has been considered untreatable," Oswald Steward, a professor of anatomy and neurobiology at University of California, Irvine and co-author of the new paper, said in a prepared statement. "Our discovery points the way toward a potential therapy to induce regeneration of nerve connections following spinal cord injury in people."

Image courtesy of Wikimedia Commons/David Mcllwain/Victoria Hoke

*Correction (8/9/10): This sentence was changed after publication. It originally stated that the mice had regained voluntary movement. The headline was also changed to reflect this clarification.





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  1. 1. tharriss 9:56 am 08/9/2010

    Amazing! I would have liked to hear what the next steps are towards moving in the direction of an actual treatment…

    The somewhat vague "Our discovery points the way"… isn’t very encouraging as to how far off this might be in the future.

    Link to this
  2. 2. stemcellblogger 11:27 am 08/9/2010

    Stepping Towards A Paralysis Cure, A Tale Of Two Supermen Stem Cells Cure 23 Year Old Male of Paralysis C6-C7 injury http://repairstemcell.wordpress.com/2009/03/28/stepping-towards-a-paralysis-cure-a-tale-of-two-supermen-stem-cells-cure-23-year-old-male-of-paralysis-c6-c7-injury/

    Link to this
  3. 3. stemcellblogger 11:27 am 08/9/2010

    Stepping Towards A Paralysis Cure, A Tale Of Two Supermen Stem Cells Cure 23 Year Old Male of Paralysis – C6-C7 injury
    http://repairstemcell.wordpress.com/2009/03/28/stepping-towards-a-paralysis-cure-a-tale-of-two-supermen-stem-cells-cure-23-year-old-male-of-paralysis-c6-c7-injury/

    Link to this
  4. 4. ironjustice 9:01 am 08/10/2010

    Iron is a substrate for enzymes. Targeting iron has been shown to result in functional recovery after spinal cord injury. Could? the simple fact iron is released when there is trauma BE the ‘activator’ OF this enzyme and would NORMALLY be removed during an injury but when the iron is NOT removed it continues in its’ BEING a ‘substrate’ FOR the enzyme ? One might wonder if any types of metal chelators would / could disallow the enzyme FROM ‘being’ .. ?

    Link to this
  5. 5. ironjustice 5:29 pm 08/10/2010

    Quote: One might wonder if any types of metal chelators would / could disallow the enzyme FROM ‘being’ .. ?
    Answer: Looks like it might be a valid strategy ?
    " These new therapeutic strategies include the use of agents that target iron to inhibit proliferation via multiple mechanisms and suppression of AKT by cytosolic phospholipase A(2)-alpha inhibitors."

    Link to this

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