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One big step for Geron: Therapy that enabled paralyzed rats to walk ready for test on humans, stem-cell firm says

February 24, 2008

(Editor’s note: This will have implications for Dejerine-Sottas research in the future:)
Using human embryonic stem cells, the Menlo Park company has developed a therapy that enables paralyzed rats to walk and that it claims shows no dangerous side effects in experiments with about 2,000 animals.
Others also are studying such cells for medical uses, including Stanford University scientists, who last week said they had used them to help stroke-disabled lab rats walk better. But none are as close to seeking permission for human tests as Geron, whose treatment is for spinal injuries.
For its application requesting regulatory approval from the U.S. Food and Drug Administration, the public company has gathered 25,000 pages of data – far more than normal for such requests, Geron Chief Executive Dr. Thomas Okarma said. He told analysts recently that Geron would submit it to the FDA during the first part of this year. But he declined to reveal the actual filing date, he said, “to minimize any kind of pressure on the agency.”
Yet Geron’s bid isn’t certain.
Although the FDA would not comment on Geron’s application, President Bush objects to most research with embryonic stem cells, which come from discarded embryos. Moreover, his administration has become intrigued with recent studies showing skin cells can be manipulated to have embryonic-like properties without harming an embryo.
Read the rest of One Big Step for Geron.

The neuropathic pain triad: neurons, immune cells and glia

February 5, 2008

Nat Neurosci. 2007 Nov;10(11):1361-8.
Scholz J, Woolf CJ.
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Nociceptive pain results from the detection of intense or noxious stimuli by specialized high-threshold sensory neurons (nociceptors), a transfer of action potentials to the spinal cord, and onward transmission of the warning signal to the brain. In contrast, clinical pain such as pain after nerve injury (neuropathic pain) is characterized by pain in the absence of a stimulus and reduced nociceptive thresholds so that normally innocuous stimuli produce pain. The development of neuropathic pain involves not only neuronal pathways, but also Schwann cells, satellite cells in the dorsal root ganglia, components of the peripheral immune system, spinal microglia and astrocytes. As we increasingly appreciate that neuropathic pain has many features of a neuroimmune disorder, immunosuppression and blockade of the reciprocal signaling pathways between neuronal and non-neuronal cells offer new opportunities for disease modification and more successful management of pain.

Developmental loss of NT-3 in vivo results in reduced levels of myelin-specific proteins

February 1, 2008

Glia. 2008 Feb;56(3):306-17.
Developmental loss of NT-3 in vivo results in reduced levels of myelin-specific proteins, a reduced extent of myelination and increased apoptosis of Schwann cells.
Woolley AG, Tait KJ, Hurren BJ, Fisher L, Sheard PW, Duxson MJ.
Department of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
This work investigates the role of NT-3 in peripheral myelination. Recent articles, based in vitro, propose that NT-3 acting through its high-affinity receptor TrkC may act to inhibit myelin formation by enhancing Schwann cell motility and/or migration. Here, we investigate this hypothesis in vivo by examining myelination formation in NT-3 mutant mice. On the day of birth, soon after the onset of myelination, axons showed normal ensheathment by Schwann cells, no change in the proportion of axons which had begun to myelinate, and no change in either myelin thickness or number of myelin lamellae. However in postnatal day 21 mice, when myelination is substantially complete, we observed an unexpected reduction in mRNA and protein levels for MAG and P(0), and in myelin thickness. This is the opposite result to that predicted from previous in vitro studies, where removal of an inhibitory NT-3 signal would have been expected to enhance myelination. These results suggest that, in vivo, the importance of NT-3 as a major support factor for Schwann cells (Meier et al., (1999) J Neurosci 19:3847-3859) over-rides its potential role as an myelin inhibitor, with the net effect that loss of NT-3 results in degradation of Schwann cell functions, including myelination. In support of this idea, Schwann cells of NT-3 null mutants showed increased expression of activated caspase-3. Finally, we observed significant reduction in width of the Schwann cell periaxonal collar in NT-3 mutant animals suggesting that loss of NT-3 and resulting reduction in MAG levels may alter signaling at the axon-glial interface.