Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 151-160 of 1,773 results
Glia, 2014 • December 1, 2014
The study compared behavioral outcome, axonal remodeling, and CSPG expression between wild-type (WT) and GFAP−/−Vim−/− mice after stroke. Motor functional recovery and CST axonal length were significa...
KEY FINDING: GFAP−/−Vim−/− mice exhibited reduced motor functional recovery and BDA-positive CST axonal length compared to WT mice after stroke.
Int. J. Mol. Sci., 2014 • July 25, 2014
Spinal cord injury (SCI) results in neuronal and glial death and the loss of axons at the injury site. Inflammation after SCI leads to the inhibition of tissue regeneration and reduced neuronal surviv...
KEY FINDING: RAGE and its ligands appears to contribute to the inflammatory response caused by SCI by regulating the secretion of cytokines and chemokines and modulating apoptosis signaling
PLoS ONE, 2014 • August 6, 2014
This study investigates the role of b1-integrin signaling in regulating astrocytic differentiation of neural stem cells after nervous system injury, focusing on glial scar formation. The research demo...
KEY FINDING: b1-integrin signaling suppresses astrocytic differentiation of both cultured ependymal stem cells (ESCs) and subventricular zone (SVZ) progenitor cells.
Neuroreport, 2014 • October 22, 2014
The study investigated the expression of Nav1.5 in astrocytes in mouse models of multiple sclerosis (MS), specifically monophasic and chronic-relapsing experimental autoimmune encephalomyelitis (EAE)....
KEY FINDING: Nav1.5 is upregulated in astrocytes in situ in a temporal manner that correlates with disease severity in both monophasic and chronic-relapsing EAE.
Neural Regen Res, 2013 • January 1, 2013
This study investigated the role of ATP-activated mTOR signaling in the physiology and pathology of SCI, with a special focus on molecular targets of upstream, downstream, and inhibitor of mTOR kinase...
KEY FINDING: ATP promotes locomotor recovery after spinal cord injury in rats, as demonstrated by improved BBB scores in the ATP group compared to control groups.
Neural Regen Res, 2013 • August 1, 2013
This study investigates the temporal and spatial changes in the expression of protein disulfide isomerase A3, stress-induced-phosphoprotein 1 and heat shock cognate protein 70 in rabbit spinal cords a...
KEY FINDING: Hind limb function initially improves after spinal cord ischemia/reperfusion injury but deteriorates later.
Neural Regen Res, 2014 • January 1, 2014
This study examined the effects of type-2 astrocytes on the survival and growth of dorsal root ganglion neurons in vitro. The results indicate that co-culture with type-2 astrocytes can increase neuro...
KEY FINDING: Co-culture with type-2 astrocytes increased the number of dorsal root ganglion neurons compared to culturing neurons alone.
Neural Regen Res, 2014 • February 1, 2014
This review discusses the extracellular matrix (ECM) and its role in axonal outgrowth regulation following central nervous system (CNS) injury, focusing on proteoglycan structure and function. It high...
KEY FINDING: Specific receptors for CSPGs have been identified, suggesting that CSPGs inhibit axon growth through multiple mechanisms, opening new avenues for therapeutic development.
Neural Regen Res, 2014 • February 1, 2014
Proteoglycans (PGs) in the central nervous system play integral roles as “traffic signals” for the direction of neurite outgrowth. The review further describes the methods routinely used to determine ...
KEY FINDING: Proteoglycans (PGs) in the central nervous system play integral roles as “traffic signals” for the direction of neurite outgrowth, influencing regeneration after injury.
Neural Regeneration Research, 2014 • March 1, 2014
This novel technology has opened new therapeutic opportunities to generate stem cells in any tissue for cell replacement therapy in a number of disorders. Cell reprogramming technology provides a nove...
KEY FINDING: Somatic mammalian cells can be epigenetically reprogrammed to induced pluripotent stem cells (iPSCs) through the exogenous expression of the Oct4, Sox2, Klf4 and c-Myc (OSKM).