Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 761-770 of 1,773 results
The Journal of Neuroscience, 2016 • August 10, 2016
The study investigates the role of miR-155 in spinal cord injury repair, focusing on its impact on both neuron-intrinsic and neuron-extrinsic mechanisms. The research demonstrates that miR-155 deletio...
KEY FINDING: Deleting miR-155 attenuates inflammatory signaling in macrophages, reduces macrophage-mediated neuron toxicity, and increases macrophage-elicited axon growth.
Neurobiol Dis., 2015 • February 1, 2015
The study investigated the role of neutrophil elastase (NE) in acute and chronic outcomes after traumatic brain injury (TBI) in the developing brain of mice. Results showed that NE contributes to acut...
KEY FINDING: Genetic deletion or inhibition of NE results in alleviation of acute cell death, strongly implicating NE in early post-injury pathogenesis.
PLoS ONE, 2014 • December 22, 2014
This study investigated the impact of minimal-dose electrical stimulation on gene regulation in paralyzed human muscle after spinal cord injury (SCI). The key finding was that acute electrical stimula...
KEY FINDING: Acute stimulation of paralyzed muscle regulates over 100 biological pathways as compared to less than 30 in chronically trained muscle.
Exp Neurol, 2015 • March 1, 2015
This study investigates the association of microRNAs (miRNAs) with hippocampal mitochondria and changes in their expression following controlled cortical impact (CCI) injury in rats. The findings demo...
KEY FINDING: The miRNA processing proteins Argonaute (AGO) and Dicer are present in mitochondria fractions from uninjured rat hippocampus, suggesting functional RNA-induced silencing complexes are present.
Ann Rehabil Med, 2016 • August 1, 2016
This study demonstrates that following spinal cord injury (SCI), astrocyte proliferation occurs in the hippocampus, and motor neuron cell death occurs in the motor cortex. The study also found signifi...
KEY FINDING: BDNF expression was significantly elevated at 2 weeks after injury.
Glia, 2015 • May 1, 2015
Here we show that the thrombin receptor is an essential intrinsic suppressor of spinal cord myelination. Deletion of the gene encoding the thrombin receptor resulted in spinal cord hypermyelination, i...
KEY FINDING: PAR1 gene deletion resulted in earlier onset of spinal cord myelination and higher levels of proteolipid protein (PLP) at birth.
Scientific Reports, 2016 • September 27, 2016
This study investigates the role of HB-GAM in reversing the inhibitory effects of the CNS extracellular matrix on neural regeneration. It demonstrates that HB-GAM promotes neurite outgrowth by interac...
KEY FINDING: HB-GAM promotes neurite outgrowth on CSPG substrates, overcoming the inhibitory effects of aggrecan, neurocan, and brain-derived CSPGs.
JOURNAL OF NEUROTRAUMA, 2017 • February 1, 2017
The study found that HMGB1 is elevated systemically in persons with acute or chronic traumatic SCI. HMGB1 levels in acute SCI were significantly higher than in uninjured persons and more than two-fold...
KEY FINDING: HMGB1 levels are significantly elevated in individuals with acute SCI within 0-3 days and 4-7 days post-injury, compared to uninjured controls.
The Journal of Neuroscience, 2015 • March 11, 2015
This study investigates the role of complement C1q in neurite outgrowth in vitro and axon regeneration in vivo after spinal cord injury (SCI). The findings demonstrate that C1q increases neurite lengt...
KEY FINDING: Complement C1q increases neurite length on myelin in vitro, rescuing neurons from myelin-mediated growth inhibition.
Mol Cell Neurosci, 2015 • September 1, 2015
This study elucidates the regulatory mechanisms governing NRG1 expression in motor neurons, demonstrating the importance of axon-target interactions and neurotrophic factors. The findings reveal that ...
KEY FINDING: Axon-target interactions regulate NRG1 mRNA expression during early development, suggesting a trophic role from the developing limb.