scholarly journals Calpeptin attenuated inflammation, cell death, and axonal damage in animal model of multiple sclerosis

2010 ◽  
pp. NA-NA ◽  
Author(s):  
M. Kelly Guyton ◽  
Arabinda Das ◽  
Supriti Samantaray ◽  
Gerald C. Wallace ◽  
Jonathan T. Butler ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Cell Death ◽  
Axonal Damage

AIM2 inflammasome activation in astrocytes occurs during the late phase of EAE

2021 ◽  
Author(s):  
William E. Barclay ◽  
M. Elizabeth Deerhake ◽  
Makoto Inoue ◽  
Toshiaki Nonaka ◽  
Kengo Nozaki ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Animal Model ◽  
Cell Death ◽  
Nervous System ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Inflammasome Activation ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Experimental Autoimmune

ABSTRACTInflammasomes are a class of innate immune signaling platforms that activate in response to an array of cellular damage and pathogens. Inflammasomes promote inflammation under many circumstances to enhance immunity against pathogens and inflammatory responses through their effector cytokines, IL-1β and IL-18. Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are such autoimmune conditions influenced by inflammasomes. Despite work investigating inflammasomes during EAE, little remains known concerning the role of inflammasomes in the central nervous system (CNS) during the disease. Here we use multiple genetically modified mouse models to monitor activated inflammasomes in situ based on ASC oligomerization in the spinal cord. Using inflammasome reporter mice, we found heightened inflammasome activation in astrocytes after the disease peak. In contrast, microglia and CNS-infiltrated myeloid cells had few activated inflammasomes in the CNS during EAE. Astrocyte inflammasome activation was dependent on AIM2, but low IL-1β expression and no significant signs of cell death were found in astrocytes during EAE. Thus, the AIM2 inflammasome activation in astrocytes may have a distinct role from traditional inflammasome-mediated inflammation.SIGNIFICANCE STATEMENTInflammasome activation in the peripheral immune system is pathogenic in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, inflammasome activity in the central nervous system (CNS) is largely unexplored. Here, we used genetically modified mice to determine inflammasome activation in the CNS during EAE. Our data indicated heightened AIM2 inflammasome activation in astrocytes after the disease peak. Unexpectedly, neither CNS-infiltrated myeloid cells nor microglia were the primary cells with activated inflammasomes in SC during EAE. Despite AIM2 inflammasome activation, astrocytes did not undergo apparent cell death and produced little of the proinflammatory cytokine, IL-1β, during EAE. This study showed that CNS inflammasome activation occurs during EAE without associating with IL-1β-mediated inflammation.

Axonal damage and protection during early remyelination in multiple sclerosis and an animal model

2014 ◽  
Vol 275 (1-2) ◽  
pp. 129
Author(s):  
Verena Schultz ◽  
Uta Scheidt ◽  
Franziska Paap ◽  
Wolfgang Brück ◽  
Andreas Junker
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Axonal Damage

scholarly journals Neuroprotective Effect of Glatiramer Acetate on Neurofilament Light Chain Leakage and Glutamate Excess in an Animal Model of Multiple Sclerosis

2021 ◽  
Vol 22 (24) ◽  
pp. 13419
Author(s):  
Rina Aharoni ◽  
Raya Eilam ◽  
Shaul Lerner ◽  
Efrat Shavit-Stein ◽  
Amir Dori ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Cell Death ◽  
Glatiramer Acetate ◽  
Clinical Symptoms ◽  
Apoptotic Cell ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Neurofilament Light Chain ◽  
Neurofilament Light

Axonal and neuronal pathologies are a central constituent of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), induced by the myelin oligodendrocyte glycoprotein (MOG) 35–55 peptide. In this study, we investigated neurodegenerative manifestations in chronic MOG 35–55 induced EAE and the effect of glatiramer acetate (GA) treatment on these manifestations. We report that the neuronal loss seen in this model is not attributed to apoptotic neuronal cell death. In EAE-affected mice, axonal damage prevails from the early disease phase, as revealed by analysis of neurofilament light (NFL) leakage into the sera along the disease duration, as well as by immunohistological examination. Elevation of interstitial glutamate concentrations measured in the cerebrospinal fluid (CSF) implies that glutamate excess plays a role in the damage processes inflicted by this disease. GA applied as a therapeutic regimen to mice with apparent clinical symptoms significantly reduces the pathological manifestations, namely apoptotic cell death, NFL leakage, histological tissue damage, and glutamate excess, thus corroborating the neuroprotective consequences of this treatment.

The Voltage-Gated Sodium Channel Nav1.2 Contributes to Neurodegeneration in an Animal Model of Multiple Sclerosis

2016 ◽  
Vol 47 (S 01) ◽  
Author(s):  
W. Fazeli ◽  
B. Schattling ◽  
B. Engeland ◽  
M. Friese ◽  
D. Isbrand
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Sodium Channel ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated

scholarly journals Main Role of Antibodies in Demyelination and Axonal Damage in Multiple Sclerosis

2021 ◽  
Author(s):  
Ursula Muñoz ◽  
Cristina Sebal ◽  
Esther Escudero ◽  
Margaret Esiri ◽  
John Tzartos ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Axonal Damage ◽  
Main Role

The brain 3β-HSD up-regulation in response to deteriorating effects of background emotional stress: an animal model of multiple sclerosis

2021 ◽  
Author(s):  
Sogol Meknatkhah ◽  
Monireh-Sadat Mousavi ◽  
Pouya Sharif Dashti ◽  
Leila Azizzadeh Pormehr ◽  
Gholam Hossein Riazi
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Emotional Stress ◽  
The Brain

B cells from patients with multiple sclerosis induce cell death via apoptosis in neurons in vitro

2017 ◽  
Vol 309 ◽  
pp. 88-99 ◽  
Author(s):  
Robert P. Lisak ◽  
Liljana Nedelkoska ◽  
Joyce A. Benjamins ◽  
Dana Schalk ◽  
Beverly Bealmear ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cell Death ◽  
B Cells ◽  
Induce Cell Death

Putting Magnetic Resonance Spectroscopy Studies in Context: Axonal Damage and Disability in Multiple Sclerosis

1998 ◽  
Vol 18 (03) ◽  
pp. 327-336 ◽  
Author(s):  
P. Matthews ◽  
N. De Stefano ◽  
S. Narayanan ◽  
G. Francis ◽  
J. Wolinsky ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Axonal Damage ◽  
Resonance Spectroscopy ◽  
Spectroscopy Studies
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