Browse the latest research summaries in the field of neurology for spinal cord injury patients and caregivers.
Showing 5,301-5,310 of 5,401 results
The Journal of Neuroscience, 2009 • July 8, 2009
This study re-evaluated the role of Nogo, a myelin-derived neurite growth inhibitor, in corticospinal tract (CST) regeneration after spinal cord injury in mice, addressing inconsistencies in previous ...
KEY FINDING: Neither the reanalyzed Nogo-A,B gene-trap mutant nor the novel Nogo deletion mutant exhibited enhanced corticospinal tract (CST) regeneration after experimental spinal cord injury.
PLoS ONE, 2009 • July 14, 2009
This study demonstrates that lentiviral-mediated RNAi can efficiently silence GFAP and vimentin expression in cultured astrocytes. The use of Lv-shGFAP and Lv-shVIM vectors resulted in a significant d...
KEY FINDING: Lv-shGFAP and Lv-shVIM vectors effectively silenced GFAP and vimentin expression in cultured astrocytes.
Biotechnol Bioeng, 2009 • December 15, 2009
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. The additi...
KEY FINDING: The addition of 500 ng/ mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone.
Molecular Therapy, 2009 • July 21, 2009
The study demonstrates that lentiviral delivery of DNROCK to neurons can effectively target the RhoA-ROCK signal pathway, promoting regenerative sprouting of injured axons after CNS injury. DNROCK enh...
KEY FINDING: DNROCK expression in DRG neurons promotes neurite growth on myelin proteins in vitro, overcoming the inhibitory effects of CNS myelin.
JOURNAL OF NEUROTRAUMA, 2009 • December 1, 2009
This study investigates the efficacy of FTY720, an immunomodulatory drug, in reducing inflammation and promoting functional recovery in a rat model of spinal cord injury (SCI). The hypothesis is that ...
KEY FINDING: FTY720 treatment significantly reduced the infiltration of CD4+ T-helper cells and CD8+ cytotoxic T-cells into the spinal cord lesion site after injury, as shown by flow cytometry.
Nat Neurosci, 2009 • September 1, 2009
This study demonstrates the reinnervation of brainstem targets after SCI and the essential role of chemotropic axon guidance in target selection. Regenerating axons in the injured adult CNS utilized c...
KEY FINDING: NT-3 expression in the correct target (nucleus gracilis) led to reinnervation in a dose-related fashion.
JOURNAL OF NEUROTRAUMA, 2009 • October 1, 2009
This study evaluated the effect of buprenorphine on molecular, behavioral, electrophysiological, and histological levels after SCI in rats. The rats were injured at the T10 thoracic level and half rec...
KEY FINDING: Microarray analysis showed no significant difference in gene expression between rats treated with buprenorphine and the control group at 2 and 4 days post-injury (DPI).
Respir Physiol Neurobiol, 2009 • November 30, 2009
Neural and non-neural tissue and cell transplantation have been used to study CNS injury mechanisms, plasticity, regeneration, and recovery of function. Successful functional recovery after CNS injuri...
KEY FINDING: Peripheral nerve transplantation can promote CNS axon regeneration if the environment is suitable.
Genesis, 2009 • November 1, 2009
This study generated an allelic series of OMgp in mice to investigate its role in axon regeneration. The series includes a null allele with a LacZ reporter, a clean null allele, and a conditional alle...
KEY FINDING: The study successfully generated an OMgp allelic series in mice, including a null allele with a LacZ reporter, one without a reporter gene (clean null), and a conditional allele.
Glia, 2010 • February 1, 2010
This study investigates the molecular mechanisms underlying the upregulation of CHL1 expression in reactive astrocytes following spinal cord injury (SCI). It demonstrates that bacterial lipopolysaccha...
KEY FINDING: LPS upregulates CHL1 expression in astrocytes via a PI3K/PKCδ-dependent pathway.