Browse the latest research summaries in the field of regenerative medicine for spinal cord injury patients and caregivers.
Showing 2,141-2,150 of 2,298 results
The Journal of Neuroscience, 2006 • May 3, 2006
After treatment with antibodies that bind to and neutralize specifically the NG2 proteoglycan, medium- and large-diameter mechanosensory axons grow into the growth nonpermissive environment of the gli...
KEY FINDING: Treatment of acute spinal cord injuries with antibodies that neutralize NG2 function can promote the regeneration of ascending mechanosensory axons.
The Journal of Neuroscience, 2006 • May 17, 2006
The study compares the gene expression profiles of three OEC populations that differ in their capacity to promote adult axonal regeneration in vitro to identify molecules that OECs use to promote axon...
KEY FINDING: MMP2 and its inhibitor Timp2 are candidate molecules that may promote and inhibit axonal regeneration, respectively. MMP2 was found to be present in medium conditioned by primary and TEG3 OECs, whereas MMP2 was barely detected in OEC Lp conditioned medium.
The Journal of Neuroscience, 2006 • May 24, 2006
This study investigates the impact of Nogo-A deletion on axonal regeneration in two different mouse strains, 129X1/SvJ and C57BL/6, following spinal cord injury. The findings demonstrate that Nogo-A d...
KEY FINDING: Nogo-A-deficient mice displayed enhanced regeneration of the corticospinal tract after injury, confirming Nogo-A's role as an inhibitor of axonal regeneration.
Cellular and Molecular Neurobiology, 2006 • June 16, 2006
This study investigates the potential of using transdifferentiated mesenchymal stem cells (MSCs) to promote nerve regeneration and myelination. Demyelination is a critical factor in various neurologic...
KEY FINDING: Transdifferentiated MSCs can myelinate PC12 cells in vitro, similar to Schwann cells, but the degree of myelination depends on the culture medium used.
The Journal of Neuroscience, 2006 • July 12, 2006
The study demonstrates that modulation of extracellular matrix components promotes significant axonal regeneration beyond a PN bridge back into the spinal cord. Regenerating axons can mediate the retu...
KEY FINDING: ChABC treatment enhanced axonal regrowth from the PN graft into the spinal cord.
PNAS, 2006 • July 18, 2006
The injured CNS limits functional recovery due to axon regeneration inhibitors (ARIs). Reversing ARI action may enhance axon outgrowth and recovery after CNS injury. Sialidase or chondroitinase ABC en...
KEY FINDING: Infusion of Clostridium perfringens sialidase to the injury site markedly increased the number of spinal axons that grew into the graft.
Nat Rev Neurosci, 2006 • August 1, 2006
The review discusses the inhibitory molecules in the adult CNS environment responsible for regenerative failure after injury. These inhibitors are associated with later stages of nervous system develo...
KEY FINDING: CNS myelin and glial scars inhibit axon outgrowth, but their relative importance in vivo is uncertain. Myelin inhibitors are constitutively expressed, while CSPGs are strongly upregulated following injury, with different time courses of expression ranging from 24 hours to 6 months post-lesion.
J Comp Neurol, 2006 • October 1, 2006
The study investigates the fate of endogenous stem/progenitor cells following spinal cord injury (SCI) in adult rats and mice. It demonstrates that constitutively dividing progenitor cells are vulnera...
KEY FINDING: Constitutively proliferating adult progenitor cells are vulnerable to spinal cord injury, leading to their death or reduced proliferation.
Phil. Trans. R. Soc. B, 2006 • July 28, 2006
The adult mammalian CNS does not spontaneously regenerate after injury due to an inhibitory environment and changes in the neurons themselves. This contrasts with the neonatal CNS, which can regenerat...
KEY FINDING: The glial scar, formed by reactive astrocytes, is a major component of the inhibitory environment in the adult CNS. These astrocytes express inhibitory chondroitin sulphate proteoglycans (CSPGs).
J Neurobiol, 2006 • December 1, 2006
This study demonstrates that the mechanism of axon regeneration undergoes a developmental switch between E7 and E14 from strict dependence on F-actin to a greater dependence on microtubule polymerizat...
KEY FINDING: Early embryonic (E7) sensory axons strictly require F-actin for axon maintenance and regeneration, whereas later embryonic (E14) axons can extend even in the absence of F-actin.