Browse the latest research summaries in the field of neurology for spinal cord injury patients and caregivers.
Showing 231-240 of 5,401 results
Auton Neurosci, 2013 • December 1, 2013
The study examined the effects of cervical sympathetic trunk (CST) transection on sympathetic preganglionic neurons, focusing on changes in ChAT expression, soma size, and the presence of ATF3 in the ...
KEY FINDING: Significant decrease in soma volume and reduced soma expression of choline acetyltransferase (ChAT) in the intermediolateral cell column (IML) of T1 spinal cord were observed at 1 week.
Exp Neurol, 2013 • October 1, 2013
This study examined the pre-clinical potential of NPCs derived from human induced pluripotent stem cells (hiPSCs) to repair chronic SCI. hiPSCs were differentiated into region-specific (i.e. caudal) N...
KEY FINDING: Caudalized hiPSC-NPCs can be successfully transplanted into an early chronic cervical SCI model and survive for up to two months post-transplant without risk of overgrowth or loss of function.
Cell Mol Neurobiol, 2013 • July 28, 2013
This study aimed to determine if Wnt signaling-activated olfactory ensheathing cells (wOECs) can promote synaptogenesis and neurite growth in vitro, comparing them to control OECs and Wnt-inhibited OE...
KEY FINDING: Wnt-activated OECs (wOECs CM) exhibited a stronger axonal growth-promoting effect than control OECs CM (cOECs CM).
Neurosci Bull, 2013 • August 1, 2013
This review provides an overview of different animal models used in spinal cord injury research, specifically focusing on axon regeneration. It discusses the pros and cons of each model, including con...
KEY FINDING: Rat models mimic human SCI pathology better due to the formation of cystic cavities, making them suitable for preclinical studies of cellular and pharmacological therapies.
Neurosci Bull, 2013 • August 1, 2013
Membrane disruption has serious downstream structural and functional consequences in the mechanical injury of neuronal tissue. PEG-mediated resealing of cell membranes is a practical method to repair ...
KEY FINDING: Polyethylene glycol (PEG) can reseal axonal membranes following various injuries in multiple in vitro and in vivo injury models.
Neurosci Bull, 2013 • August 1, 2013
This review provides an overview of the anatomical and electrophysiological changes occurring within the spinal cord that lead to, or are associated with the re-expression of locomotion in spinally-tr...
KEY FINDING: Salamanders can recover locomotor function after complete spinal cord transection due to the regeneration of descending pathways.
EMBO reports, 2013 • August 9, 2013
The study investigates the role of STAT3 in corticospinal tract (CST) remodeling after spinal cord injury (SCI). It finds that sustained activation of STAT3 enhances remodeling of lesioned CST fibers ...
KEY FINDING: Endogenous STAT3 expression after spinal cord injury is transient and does not significantly contribute to axonal remodeling.
PLoS ONE, 2013 • July 23, 2013
This study demonstrates that P45, a member of the death domain superfamily, interacts with FADD and diminishes Fas-FADD mediated death signaling. The DED of FADD is required for the complex formation ...
KEY FINDING: P45 forms a complex with FADD, and the DED domain of FADD is required for this interaction.
PLoS ONE, 2013 • August 2, 2013
This study investigates the role of SnoN, a developmentally-regulated transcription factor, in promoting axonal regeneration after spinal cord injury. The research aims to address the limited growth c...
KEY FINDING: SnoN overexpression in adult DRG neurons significantly enhances neurite growth in vitro.
The Journal of Neuroscience, 2013 • August 14, 2013
The study investigates the role of NMNAT2 in axon development and maintenance using a Nmnat2 gene-trap mouse model. Homozygous Nmnat2-deficient mice exhibit severe peripheral nerve and CNS axon defect...
KEY FINDING: NMNAT2 is essential for axon extension in both the peripheral and central nervous systems during development. NMNAT2-deficient embryos exhibit truncated axons, indicating a failure of axons to extend properly.