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1. Full Text Acute axonal damage in three different murine models of multiple sclerosis: a comparative approach
by Höflich, Katharina Marie and Beyer, Cordian and Clarner, Tim and Schmitz, Christoph and Nyamoya, Stella and Kipp, Markus and Hochstrasser, Tanja
Brain Research, ISSN 0006-8993, 2016, Volume 1650, pp. 125 - 133
Abstract Axonal damage has been identified as a significant contributor to permanent clinical disability in multiple sclerosis. In the context of demyelinating... 
Neurology | Lysolecithin | Experimental autoimmune encephalomyelitis | APP | Axonal damage | Cuprizone | C57BL/6 MICE | AMYLOID PRECURSOR PROTEIN | KINESIN LIGHT-CHAIN | NEUROSCIENCES | TRAUMATIC BRAIN-INJURY | CORPUS-CALLOSUM | IN-VIVO | GLATIRAMER ACETATE | FOCAL DEMYELINATION | CUPRIZONE-INDUCED DEMYELINATION | Immunohistochemistry | Demyelinating Diseases - physiopathology | Microglia - metabolism | Encephalomyelitis, Autoimmune, Experimental - pathology | Spinal Cord - metabolism | Myelin Sheath - pathology | Mice, Inbred C57BL | Nerve Degeneration - physiopathology | Axons - metabolism | Brain - metabolism | Cuprizone - metabolism | Multiple Sclerosis - physiopathology | Inflammation - metabolism | Animals | Cuprizone - pharmacology | Corpus Callosum - pathology | Amyloid beta-Protein Precursor - metabolism | Models, Animal | Mice | Multiple sclerosis | Amyloid beta-protein | Models | T cells | Comparative analysis | Glutamate | Neurophysiology
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2. Full Text NLR members NLRC4 and NLRP3 mediate sterile inflammasome activation in microglia and astrocytes
by Freeman, Leslie and Guo, Haitao and David, Clément N and Brickey, W. June and Jha, Sushmita and Ting, Jenny P.-Y
Journal of Experimental Medicine, ISSN 0022-1007, 05/2017, Volume 214, Issue 5, pp. 1351 - 1370
Inflammation in the brain accompanies several high-impact neurological diseases including multiple sclerosis (MS), stroke, and Alzheimer's disease.... 
MEDICINE, RESEARCH & EXPERIMENTAL | AIM2 INFLAMMASOME | III SECRETION APPARATUS | MULTIPLE-SCLEROSIS | ALZHEIMERS-DISEASE | LYSOPHOSPHATIDYL CHOLINE | CENTRAL-NERVOUS-SYSTEM | IMMUNOLOGY | IMMUNE RECOGNITION | CUPRIZONE-INDUCED DEMYELINATION | CELL-DEATH | NALP3 INFLAMMASOME | Astrocytes - drug effects | Inflammation - pathology | Microglia - drug effects | Mice, Inbred C57BL | Astrocytes - pathology | Lysophosphatidylcholines - metabolism | Male | Mice, Knockout | Inflammasomes - physiology | Astrocytes - physiology | Animals | Microglia - physiology | Cuprizone - pharmacology | Calcium-Binding Proteins - physiology | Microglia - pathology | Apoptosis Regulatory Proteins - physiology | Mice | NLR Family, Pyrin Domain-Containing 3 Protein - physiology | Disease Models, Animal | Inflammation - physiopathology | Brain | Multiple sclerosis | Calcium | Caspase-11 | Activation | Lysophosphatidylcholine | Caspase-1 | Microorganisms | Cuprizone | Neurodegeneration | Demyelination | Efflux | Stroke | Calcium mobilization | Astrocytes | Caspase | Inflammation | Microglia | Damage patterns | Neurological diseases | Gliosis | Calcium efflux | Speck | Potassium | Apoptosis | 306
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3. Full Text Demyelination reduces brain parenchymal stiffness quantified in vivo by magnetic resonance elastography
by Katharina Schregel and Eva Wuerfel née Tysiak and Philippe Garteiser and Ines Gemeinhardt and Timour Prozorovski and Orhan Aktas and Hartmut Merz and Dirk Petersen and Jens Wuerfel and Ralph Sinkus
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2012, Volume 109, Issue 17, pp. 6650 - 6655
The detection of pathological tissue alterations by manual palpation is a simple but essential diagnostic tool, which has been applied by physicians since the... 
Viscoelasticity | Pathology | Brain | Animal models | Myelination | Multiple sclerosis | Demyelinating diseases | Parenchyma | Mice | Corpus callosum | Tissue integrity | Magnetic resonance imaging | Elasticity imaging | magnetic resonance imaging | MULTIPLE-SCLEROSIS LESIONS | PRECURSOR | VISCOELASTIC PROPERTIES | AXONAL DAMAGE | MULTIDISCIPLINARY SCIENCES | CNS | elasticity imaging | CENTRAL-NERVOUS-SYSTEM | EXTRACELLULAR-MATRIX | PERINEURONAL NETS | MICE | CUPRIZONE | tissue integrity | Chelating Agents - administration & dosage | Mice, Inbred C57BL | Chelating Agents - chemistry | Elasticity Imaging Techniques - methods | Axons | Cuprizone - administration & dosage | Animals | Copper - chemistry | Brain - pathology | Female | Demyelinating Diseases - pathology | Cuprizone - chemistry | Physiological aspects | Biophysics | Research | Health aspects | Methods | Tissue | Nuclear magnetic resonance--NMR | Brain cancer | Rodents | Biological Sciences | Physical Sciences
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4. Full Text Multiple sclerosis animal models: a clinical and histopathological perspective
by Kipp, Markus and Nyamoya, Stella and Hochstrasser, Tanja and Amor, Sandra
Brain Pathology, ISSN 1015-6305, 03/2017, Volume 27, Issue 2, pp. 123 - 137
There is a broad consensus that multiple sclerosis (MS) represents more than an inflammatory disease: it harbors several characteristic aspects of a classical... 
treatment | cuprizone | PPMS | SPMS | disability | multiple sclerosis | EAE | neurodegeneration | disease progression | CORTICAL DEMYELINATION | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS | SECONDARY-PROGRESSIVE MS | PATHOLOGY | NEUROSCIENCES | CLINICAL NEUROLOGY | BIOZZI ABH MICE | APPEARING WHITE-MATTER | LYSOLECITHIN-INDUCED DEMYELINATION | MOUSE MODEL | CENTRAL-NERVOUS-SYSTEM | CUPRIZONE-INDUCED DEMYELINATION | Leukoencephalopathies - pathology | Encephalomyelitis, Autoimmune, Experimental - pathology | Neurodegenerative Diseases - pathology | Humans | Multiple Sclerosis - therapy | Disease Progression | Animals | Cuprizone - pharmacology | Spinal Cord - pathology | Axons - pathology | Multiple Sclerosis - pathology | Demyelinating Diseases - pathology | Disease Models, Animal | T cells | Multiple sclerosis | Rodents
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5. Full Text Chronic toxic demyelination in the central nervous system leads to axonal damage despite remyelination
by Lindner, Maren and Fokuhl, Jantje and Linsmeier, Franziska and Trebst, Corinna and Stangel, Martin
Neuroscience Letters, ISSN 0304-3940, 2009, Volume 453, Issue 2, pp. 120 - 125
The majority of multiple sclerosis lesions fail to remyelinate after chronic demyelinating episodes resulting in neurologic disability. In the current study,... 
Multiple sclerosis | Axonal damage | Cuprizone | Remyelination | DIAGNOSIS | MULTIPLE-SCLEROSIS LESIONS | C57BL/6 MICE | INJURY | PATHOLOGY | NEUROSCIENCES | OLIGODENDROCYTES | DEGENERATION | DISEASE | CONSEQUENCES | CUPRIZONE-INDUCED DEMYELINATION | Immunohistochemistry | Cuprizone - toxicity | Microglia - metabolism | Oligodendroglia - metabolism | Macrophages - pathology | Mice, Inbred C57BL | Nerve Fibers, Myelinated - drug effects | Axons - drug effects | Central Nervous System - pathology | Monoamine Oxidase Inhibitors - administration & dosage | Oligodendroglia - pathology | Monoamine Oxidase Inhibitors - toxicity | Cuprizone - administration & dosage | Macrophages - metabolism | Animals | Nerve Fibers, Myelinated - pathology | Axons - pathology | Central Nervous System - drug effects | Microglia - pathology | Demyelinating Diseases - chemically induced | Mice | Demyelinating Diseases - pathology | Myelin Proteins - metabolism | Neurosciences | Analysis | Myelin proteins | Index Medicus | Alzheimer's disease
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6. Full Text Low-level laser therapy modulates demyelination in mice
by Duarte, Katherine Chuere Nunes and Soares, Thaís Torres and Magri, Angela Maria Paiva and Garcia, Lívia Assis and Le Sueur-Maluf, Luciana and Renno, Ana Cláudia Muniz and Monteiro de Castro, Gláucia
Journal of Photochemistry & Photobiology, B: Biology, ISSN 1011-1344, 12/2018, Volume 189, pp. 55 - 65
There are no effective therapies for remyelination. Low-level laser therapy (LLLT) has been found advantageous in neurogenesis promotion, cell death... 
MICROGLIAL ACTIVATION | BIOPHYSICS | TRAUMATIC BRAIN-INJURY | MULTIPLE-SCLEROSIS | CNS REMYELINATION | BEHAVIORAL-CHANGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | CENTRAL-NERVOUS-SYSTEM | TOXIC DEMYELINATION | CUPRIZONE MODEL | PHOTOBIOMODULATION THERAPY | Cuprizone - administration & dosage | Low-Level Light Therapy - methods | Animals | Cuprizone - adverse effects | Oligodendrocyte Precursor Cells - cytology | Demyelinating Diseases - therapy | L-Lactate Dehydrogenase - blood | Cell Count | Demyelinating Diseases - chemically induced | Mice | Demyelinating Diseases - prevention & control | Motor Activity | Immunohistochemistry | Cell death | Lasers in surgery | Analysis | Lasers in medicine | Medical equipment | Therapy | Animal models | Toxicity | Cytotoxicity | Motors | Nervous system | Lymphocytes T | Motor task performance | Neurogenesis | Glial stem cells | Cuprizone | Lasers | Demyelination | Toxicity testing | Attenuation | Peripheral nervous system | Level (quantity) | Demyelinating diseases | Astrocytes | Feasibility studies | Lactate dehydrogenase | Continuous radiation | L-Lactate dehydrogenase | Myelination | Irradiation | Lactic acid | Apoptosis
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7. Full Text CXCR4 promotes differentiation of oligodendrocyte progenitors and remyelination
by Jigisha R. Patel and Erin E. McCandless and Denise Dorsey and Robyn S. Klein and Anthony A. James
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2010, Volume 107, Issue 24, pp. 11062 - 11067
Multiple sclerosis is a neurodegenerative disease characterized by episodes of autoimmune attack of oligodendrocytes leading to demyelination and progressive... 
Demyelinating diseases | Astrocytes | Neuroglia | Central nervous system | Oligodendroglia | Nonsense | Neural stem cells | Mice | Lentivirus | Ingestion | Chemokine | CXCL12 | Cuprizone | chemokine | cuprizone | MULTIPLE-SCLEROSIS LESIONS | MULTIDISCIPLINARY SCIENCES | PROLIFERATION | central nervous system | IN-VITRO | MOUSE MODEL | CHEMOKINE RECEPTOR | CENTRAL-NERVOUS-SYSTEM | PRECURSOR CELLS | EXPRESSION | CUPRIZONE-INDUCED DEMYELINATION | Adult Stem Cells - physiology | Chemokine CXCL12 - physiology | RNA, Small Interfering - genetics | Humans | RNA, Messenger - metabolism | Adult Stem Cells - immunology | Multiple Sclerosis - physiopathology | Oligodendroglia - immunology | Oligodendroglia - physiology | Astrocytes - immunology | RNA Interference | Base Sequence | Neuroglia - immunology | Receptors, CXCR4 - genetics | Oligodendroglia - cytology | Cell Differentiation - physiology | Chemokine CXCL12 - immunology | Disease Models, Animal | Cuprizone - toxicity | Adult Stem Cells - cytology | Myelin Sheath - physiology | Myelin Sheath - immunology | Receptors, CXCR4 - antagonists & inhibitors | Mice, Inbred C57BL | RNA, Messenger - genetics | Neuroglia - physiology | Multiple Sclerosis - genetics | Cell Differentiation - immunology | Astrocytes - physiology | Receptors, CXCR4 - physiology | Animals | Chelating Agents - toxicity | Corpus Callosum - immunology | Corpus Callosum - pathology | Multiple Sclerosis - immunology | Multiple Sclerosis - pathology | Nervous system diseases | Medical examination | Brain cells | Development and progression | Properties | Cell differentiation | Observations | Chemokines | Brain | Neurosciences | Multiple sclerosis | Cytokines | Neurons | Gene expression | Cells | Biological Sciences
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8. Full Text Acutely damaged axons are remyelinated in multiple sclerosis and experimental models of demyelination
by Schultz, Verena and van der Meer, Franziska and Wrzos, Claudia and Scheidt, Uta and Bahn, Erik and Stadelmann, Christine and Brück, Wolfgang and Junker, Andreas
Glia, ISSN 0894-1491, 08/2017, Volume 65, Issue 8, pp. 1350 - 1360
Remyelination is in the center of new therapies for the treatment of multiple sclerosis to resolve and improve disease symptoms and protect axons from further... 
axonal damage | multiple sclerosis | remyelination | WHITE-MATTER | BRAIN-INJURY | C57BL/6 MICE | NEUROSCIENCES | AUTOIMMUNE ENCEPHALOMYELITIS | LESIONS | OLIGODENDROCYTES | MYELIN | MICROGLIA | CENTRAL-NERVOUS-SYSTEM | CUPRIZONE-INDUCED DEMYELINATION | Rats, Inbred Lew | Myelin Sheath - drug effects | Male | Glial Fibrillary Acidic Protein - metabolism | Multiple Sclerosis - chemically induced | Myelin Sheath - metabolism | Time Factors | Amyloid beta-Protein Precursor - metabolism | Statistics, Nonparametric | Microglia - pathology | Female | Demyelinating Diseases - chemically induced | Membrane Proteins - metabolism | Demyelinating Diseases - pathology | Disease Models, Animal | Cuprizone - toxicity | Microglia - drug effects | Myelin Sheath - pathology | Mice, Inbred C57BL | Rats | Monoamine Oxidase Inhibitors - toxicity | Animals | Axons - pathology | Multiple Sclerosis - pathology | Mice | Lysophosphatidylcholines - toxicity | Evolution | Multiple sclerosis | Models | Damage assessment | Correlation | Myelin | Medical services | Time measurement | Injection | Patients | Density | Silver | Axons | Myelination | Cuprizone | Demyelination | Lesions | Alzheimer's disease
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9. Full Text Olesoxime accelerates myelination and promotes repair in models of demyelination
by Magalon, Karine and Zimmer, Celine and Cayre, Myriam and Khaldi, Joseph and Bourbon, Clarisse and Robles, Isabelle and Tardif, Gwenaëlle and Viola, Angèle and Pruss, Rebecca M and Bordet, Thierry and Durbec, Pascale
Annals of Neurology, ISSN 0364-5134, 02/2012, Volume 71, Issue 2, pp. 213 - 226
Objective: Multiple sclerosis is a neurodegenerative disease characterized by episodes of immune attack of oligodendrocytes leading to demyelination and... 
PROGENITOR CELLS | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | MULTIPLE-SCLEROSIS | MOBILIZATION | OLIGODENDROCYTE PRECURSOR CELLS | RECEPTOR | SUBVENTRICULAR ZONE | DIFFERENTIATION | NEUROSCIENCES | LESIONS | CLINICAL NEUROLOGY | NERVOUS-SYSTEM REMYELINATION | Cuprizone - toxicity | Myelin Sheath - physiology | Mice, Inbred C57BL | Myelin Sheath - drug effects | Rats | Rats, Sprague-Dawley | Magnetic Resonance Imaging | Monoamine Oxidase Inhibitors - toxicity | Multiple Sclerosis - physiopathology | Animals | Oligodendroglia - drug effects | Oligodendroglia - physiology | Demyelinating Diseases - chemically induced | Mice | Cholestenones - therapeutic use | Demyelinating Diseases - drug therapy | Disease Models, Animal | Multiple Sclerosis - drug therapy | Medical research | Rodents | Monoamine Oxidase Inhibitors | Cholestenones | Cellular Biology | Multiple Sclerosis | Life Sciences | Cuprizone | Myelin Sheath | Oligodendroglia | Demyelinating Diseases
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10. Full Text Therapeutic effect of oligomeric proanthocyanidin in cuprizone‐induced demyelination
by Wang, Qing and Wang, Jing and Yang, Zhichao and Sui, Ruoxuan and Miao, Qiang and Li, Yanhua and Yu, Jiezhong and Liu, Chunyun and Zhang, Guangxian and Xiao, Baoguo and Ma, Cungen
Experimental Physiology, ISSN 0958-0670, 06/2019, Volume 104, Issue 6, pp. 876 - 886
What is the central question of this study? Oligomeric proanthocyanidin has the capacity to alleviate abnormalities in neurological functioning. However,... 
oligomeric proanthocyanidin | cuprizone‐induced | inflammatory reaction | demyelination | ANTIBODIES | PHYSIOLOGY | PROTEIN | OLIGODENDROCYTE GLYCOPROTEIN | MODEL | cuprizone-induced | MYELIN | MULTIPLE-SCLEROSIS | NEUROINFLAMMATION | MICROGLIA | DISEASE | Autoimmunity | Multiple sclerosis | T cells | Health aspects | Analysis | Myelin proteins | Oligodendrocyte-myelin glycoprotein | Autoantibodies | Seeds | Demyelinating diseases | Myelin | Secretion | Lymphocytes T | Inflammation | Corpus callosum | Myelin basic protein | Microglia | Plant extracts | Myelination | Neuromyelitis | Lymphocytes B | Cuprizone | Natural products | Neurodegeneration | Demyelination | Oligodendrocytes
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11. Full Text Quantification of increased cellularity during inflammatory demyelination
by Wang, Yong and Wang, Qing and Haldar, Justin P and Yeh, Fang-Cheng and Xie, Mingqiang and Sun, Peng and Tu, Tsang-Wei and Trinkaus, Kathryn and Klein, Robyn S and Cross, Anne H and Song, Sheng-Kwei
Brain, ISSN 0006-8950, 12/2011, Volume 134, Issue 12, pp. 3587 - 3598
Multiple sclerosis is characterized by inflammatory demyelination and irreversible axonal injury leading to permanent neurological disabilities. Diffusion... 
diffusion tensor imaging | magnetic resonance imaging | multiple tensor model | inflammation | white matter injury | APPARENT DIFFUSION | MULTIEXPONENTIAL DECAY DATA | NATURAL-HISTORY | NEUROSCIENCES | CLINICAL NEUROLOGY | MULTIPLE-SCLEROSIS | WHITE-MATTER PATHOLOGY | CORPUS-CALLOSUM | DIFFUSION MRI | MAGNETIC-RESONANCE | UNIFORM-PENALTY INVERSION | CUPRIZONE-INDUCED DEMYELINATION | Inflammation - pathology | Myelin Sheath - pathology | Trigeminal Nerve - pathology | Male | Diffusion Tensor Imaging | Magnetic Resonance Imaging | Animals | Cuprizone | Nerve Fibers, Myelinated - pathology | Corpus Callosum - pathology | Demyelinating Diseases - chemically induced | Mice | Demyelinating Diseases - pathology | Original
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