LOTUS, a possible endogenous inhibitor of axonal degeneration, as a new biomarker for multiple sclerosis

2015 ◽  
Vol 5 (6) ◽  
pp. 469-472 ◽  
Author(s):  
Keita Takahashi ◽  
Fumiaki Tanaka ◽  
Kohtaro Takei
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Degeneration ◽  
Endogenous Inhibitor

Remyelination of Demyelinated CNS Axons by Transplanted Human Schwann Cells: The Deleterious Effect of Contaminating Fibroblasts

2001 ◽  
Vol 10 (3) ◽  
pp. 305-315 ◽  
Author(s):  
C. M. H. Brierley ◽  
A. J. Crang ◽  
Y. Iwashita ◽  
J. M. Gilson ◽  
N. J. Scolding ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Axonal Degeneration ◽  
Autologous Transplantation ◽  
Growth Factor Receptor ◽  
Adult Rats ◽  
Demyelinating Lesions ◽  
Cell Implantation

Areas of demyelination can be remyelinated by transplanting myelin-forming cells. Schwann cells are the naturally remyelinating cells of the peripheral nervous system and have a number of features that may make them attractive for cell implantation therapies in multiple sclerosis, in which spontaneous but limited Schwann cell remyelination has been well documented. Schwann cells can be expanded in vitro, potentially affording the opportunity of autologous transplantation; and they might also be spared the demyelinating process in multiple sclerosis. Although rat, cat, and monkey Schwann cells have been transplanted into rodent demyelinating lesions, the behavior of transplanted human Schwann cells has not been evaluated. In this study we examined the consequences of injecting human Schwann cells into areas of acute demyelination in the spinal cords of adult rats. We found that transplants containing significant fibroblast contamination resulted in deposition of large amounts of collagen and extensive axonal degeneration. However, Schwann cell preparations that had been purified by positive immunoselection using antibodies to human low-affinity nerve growth factor receptor containing less than 10% fibroblasts were associated with remyelination. This result indicates that fibroblast contamination of human Schwann cells represents a greater problem than would have been appreciated from previous studies.

Biological markers in CSF and blood for axonal degeneration in multiple sclerosis

2005 ◽  
Vol 4 (1) ◽  
pp. 32-41 ◽  
Author(s):  
Charlotte E Teunissen ◽  
Christine Dijkstra ◽  
Chris Polman
Keyword(s):  
Multiple Sclerosis ◽  
Biological Markers ◽  
Axonal Degeneration

scholarly journals Nav1.6 promotes inflammation and neuronal degeneration in a mouse model of multiple sclerosis

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Barakat Alrashdi ◽  
Bassel Dawod ◽  
Andrea Schampel ◽  
Sabine Tacke ◽  
Stefanie Kuerten ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Retinal Ganglion Cells ◽  
Axonal Degeneration ◽  
Ganglion Cells ◽  
Neuronal Degeneration ◽  
Retinal Ganglion ◽  
Autoimmune Encephalomyelitis ◽  
Aav Vector ◽  
Α Subunit

Abstract Background In multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) model of MS, the Nav1.6 voltage-gated sodium (Nav) channel isoform has been implicated as a primary contributor to axonal degeneration. Following demyelination Nav1.6, which is normally co-localized with the Na+/Ca2+ exchanger (NCX) at the nodes of Ranvier, associates with β-APP, a marker of neural injury. The persistent influx of sodium through Nav1.6 is believed to reverse the function of NCX, resulting in an increased influx of damaging Ca2+ ions. However, direct evidence for the role of Nav1.6 in axonal degeneration is lacking. Methods In mice floxed for Scn8a, the gene that encodes the α subunit of Nav1.6, subjected to EAE we examined the effect of eliminating Nav1.6 from retinal ganglion cells (RGC) in one eye using an AAV vector harboring Cre and GFP, while using the contralateral either injected with AAV vector harboring GFP alone or non-targeted eye as control. Results In retinas, the expression of Rbpms, a marker for retinal ganglion cells, was found to be inversely correlated to the expression of Scn8a. Furthermore, the gene expression of the pro-inflammatory cytokines Il6 (IL-6) and Ifng (IFN-γ), and of the reactive gliosis marker Gfap (GFAP) were found to be reduced in targeted retinas. Optic nerves from targeted eyes were shown to have reduced macrophage infiltration and improved axonal health. Conclusion Taken together, our results are consistent with Nav1.6 promoting inflammation and contributing to axonal degeneration following demyelination.

Trans-synaptic axonal degeneration in the visual pathway in multiple sclerosis

2014 ◽  
Vol 75 (1) ◽  
pp. 98-107 ◽  
Author(s):  
Iñigo Gabilondo ◽  
Elena H. Martínez-Lapiscina ◽  
Eloy Martínez-Heras ◽  
Elena Fraga-Pumar ◽  
Sara Llufriu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Degeneration ◽  
Visual Pathway

scholarly journals Axonal degeneration of the peripheral nerves and postganglionic anhidrosis in a patient with multiple sclerosis.

1990 ◽  
Vol 162 (3) ◽  
pp. 279-291 ◽  
Author(s):  
HIROSHI SAITO ◽  
KAZUO KOBAYASHI ◽  
HIROSHI MOCHIZUKI ◽  
TOMONORI ISHII
Keyword(s):  
Multiple Sclerosis ◽  
Peripheral Nerves ◽  
Axonal Degeneration

scholarly journals The central role of mitochondria in axonal degeneration in multiple sclerosis

2014 ◽  
Vol 20 (14) ◽  
pp. 1806-1813 ◽  
Author(s):  
Graham R Campbell ◽  
Joseph T Worrall ◽  
Don J Mahad
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Degeneration ◽  
Neuronal Cell ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Autoimmune Encephalomyelitis ◽  
Mitochondrial Abnormalities ◽  
Neuronal Cell Bodies ◽  
Chain Complexes

Neurodegeneration in multiple sclerosis (MS) is related to inflammation and demyelination. In acute MS lesions and experimental autoimmune encephalomyelitis focal immune attacks damage axons by injuring axonal mitochondria. In progressive MS, however, axonal damage occurs in chronically demyelinated regions, myelinated regions and also at the active edge of slowly expanding chronic lesions. How axonal energy failure occurs in progressive MS is incompletely understood. Recent studies show that oligodendrocytes supply lactate to myelinated axons as a metabolic substrate for mitochondria to generate ATP, a process which will be altered upon demyelination. In addition, a number of studies have identified mitochondrial abnormalities within neuronal cell bodies in progressive MS, leading to a deficiency of mitochondrial respiratory chain complexes or enzymes. Here, we summarise the mitochondrial abnormalities evident within neurons and discuss how these grey matter mitochondrial abnormalities may increase the vulnerability of axons to degeneration in progressive MS. Although neuronal mitochondrial abnormalities will culminate in axonal degeneration, understanding the different contributions of mitochondria to the degeneration of myelinated and demyelinated axons is an important step towards identifying potential therapeutic targets for progressive MS.

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