Disappearing "T1 black holes" in an animal model of multiple sclerosis

10.2741/1322 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 1222 ◽  
Author(s):  
Istvan Pirko
Keyword(s):  
Multiple Sclerosis ◽  
Black Holes ◽  
Animal Model

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

An optimized animal model of lysolecithin induced demyelination in optic nerve; more feasible, more reproducible, promising for studying the progressive forms of multiple sclerosis

2021 ◽  
Vol 352 ◽  
pp. 109088
Author(s):  
Samaneh Dehghan ◽  
Ehsan Aref ◽  
Mohammad Reza Raoufy ◽  
Mohammad Javan
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Optic Nerve

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

scholarly journals Effects of Interferon Beta-1b on Black Holes in Multiple Sclerosis Over a 6-Year Period With Monthly Evaluations

2005 ◽  
Vol 62 (11) ◽  
pp. 1684 ◽  
Author(s):  
Francesca Bagnato ◽  
Shiva Gupta ◽  
Nancy D. Richert ◽  
Roger D. Stone ◽  
Joan M. Ohayon ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Black Holes ◽  
Interferon Beta

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.

RON-regulated innate immunity is protective in an animal model of multiple sclerosis

2005 ◽  
Vol 57 (6) ◽  
pp. 883-895 ◽  
Author(s):  
Shigeki Tsutsui ◽  
Farshid Noorbakhsh ◽  
Andrea Sullivan ◽  
Andrew J. Henderson ◽  
Kenneth Warren ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Innate Immunity ◽  
Animal Model

Lesion-to-ventricle distance and other risk factors for the persistence of newly formed black holes in relapsing–remitting multiple sclerosis

2013 ◽  
Vol 20 (3) ◽  
pp. 322-330 ◽  
Author(s):  
Athina Papadopoulou ◽  
Milena Menegola ◽  
Jens Kuhle ◽  
Sreeram V Ramagopalan ◽  
Marcus D’Souza ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Black Holes ◽  
Subventricular Zone ◽  
Magnetic Resonance Images ◽  
Lateral Ventricles ◽  
Relapsing Remitting ◽  
Specific Factors ◽  
One Year ◽  
Relapsing Remitting Multiple Sclerosis ◽  
The Relationship

Background: Progenitor cells from the subventricular zone (SVZ) of the lateral ventricles are assumed to contribute to remyelination and resolution of black holes (BHs) in multiple sclerosis (MS). This process may depend on the distance between the lesion and the SVZ. Objective: The objective of this paper is to investigate the relationship between lesion-to-ventricle (LV) distance and persistence of new BHs. Methods: We analysed the magnetic resonance images (MRIs) of 289 relapsing–remitting (RR) MS patients, obtained during a multi-centre, placebo-controlled phase II trial over one year. Results: Overall, 112/289 patients showed 367 new BHs at the beginning of the trial. Of these, 225 were located in 94/112 patients at the level of the lateral ventricles on axial MRIs and included in this analysis. In total, 86/225 (38%) BHs persisted at month 12. LV distance in persistent BHs (PBHs) was not longer than in transient BHs. In fact PBHs tended to be closer to the SVZ than transient BHs. A generalised linear mixed multivariate model adjusted for BHs clustered within a patient and including patient- as well as lesion-specific factors revealed size, ring contrast enhancement, and shorter LV distance as independent predictors for BH persistence. Conclusion: Location of BHs close to the lateral ventricles does not appear to favourably influence the resolution of new BHs in RRMS.

scholarly journals Treatment of a multiple sclerosis animal model by a novel nanodrop formulation of a natural antioxidant [Corrigendum]

2018 ◽  
Vol Volume 13 ◽  
pp. 4845-4846 ◽  
Author(s):  
Orli Binyamin ◽  
Liraz Larush ◽  
Kati Frid ◽  
Guy Keller ◽  
Yael Friedman-Levi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Natural Antioxidant
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