Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 1,461-1,470 of 1,773 results
Scientific Reports, 2018 • August 10, 2018
The study demonstrates that forced expression of KLF6 promotes axon regeneration in corticospinal tract neurons after spinal cord injury. RNA sequencing identified genes whose expression changed upon ...
KEY FINDING: Forced expression of KLF6 promotes axon regeneration by corticospinal tract neurons in the injured spinal cord.
Scientific Reports, 2018 • September 12, 2018
The study demonstrates that low-dose calcipotriol can induce the expression of cathelicidin, enhance wound closure, and increase local antimicrobial defense in RDEB keratinocytes in vitro. A single-pa...
KEY FINDING: Calcipotriol treatment enhanced wound closure in RDEB cell monolayers, with up to a 2-fold increase observed in scratch closure rates.
eLife, 2018 • September 11, 2018
This study investigates the role of oligodendrocyte-encoded Kir4.1 channels in maintaining white matter integrity and axonal function in the optic nerve and spinal cord during development, adulthood, ...
KEY FINDING: Kir4.1 channels are localized to perinodal areas and the inner myelin tongue, suggesting roles in juxta-axonal K+ removal.
Journal of Visualized Experiments, 2018 • September 1, 2018
The study presents a detailed protocol for in vivo electroporation of adult mouse dorsal root ganglion (DRG) to manipulate gene expression in sensory neurons. This approach enables the investigation o...
KEY FINDING: The study demonstrates a detailed protocol for in vivo electroporation of adult mouse DRG to manipulate gene expression in sensory neurons.
The Journal of Neuroscience, 2018 • October 24, 2018
This study identifies a previously unrecognized population of PNS glia that can participate in the regeneration of new myelin sheaths following CNS demyelination. The findings show that Foxj1 is also ...
KEY FINDING: A subpopulation of nonmyelinating Schwann cells identified by Foxj1 expression contributes to CNS SC remyelination, as well as remyelination in the PNS.
Cell Death & Disease, 2018 • September 3, 2018
This study reveals that Parkin and PINK1 are differentially misregulated in TDP-43 proteinopathy at both RNA and protein levels. TDP-43 downregulates Parkin mRNA via an intron-independent mechanism re...
KEY FINDING: TDP-43 overexpression reduces Parkin mRNA levels through both intron-dependent and intron-independent mechanisms.
Front. Cell. Neurosci., 2018 • September 6, 2018
This mini-review focuses on the Shh-dependent molecular mechanisms involved in the spatial and temporal control of oligodendrocyte lineage appearance. The review highlights the intricate roles of Smoo...
KEY FINDING: Shh signaling is necessary and sufficient for the expression of Olig1 and Olig2, transcription factors associated with oligodendrocyte development, in the developing neural tube.
Neural Plasticity, 2018 • August 6, 2018
This study investigated the potential of CNTF gene therapy, delivered via AAV vectors to corticospinal neurons, to promote plasticity and regeneration of axons after spinal cord injury (SCI) in adult ...
KEY FINDING: Treatment with AAV-CNTFmCherry, as well as with AAV-CNTFmCherry combined with rMPCs, yielded functional improvements over AAV-GFP alone, as assessed by open-field and Ladderwalk analyses.
Neural Regeneration Research, 2018 • December 1, 2018
This study investigates the neuroprotective effects of lithium on spinal cord injury (SCI) in rats, focusing on its potential to induce autophagy. The researchers used behavioral assessments (BBB scor...
KEY FINDING: Lithium treatment significantly improved neurological function in rats with SCI, as evidenced by higher BBB scores compared to the SCI and 3-MA groups.
The Journal of Neuroscience, 2018 • November 14, 2018
This study identifies TMEM98 as a MYRF-interacting protein that inhibits MYRF self-cleavage and nuclear translocation, thereby negatively regulating oligodendrocyte differentiation. TMEM98 is selectiv...
KEY FINDING: TMEM98 binds to the C-terminal of MYRF, preventing its self-cleavage.