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Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model
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| Zeitschriftentitel: | Annals of Clinical and Translational Neurology |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Annals of Clinical and Translational Neurology, 6, 2019, 8, S. 1362-1372 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra |
|---|---|
| author |
Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra |
| spellingShingle |
Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra Annals of Clinical and Translational Neurology Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model Neurology (clinical) General Neuroscience |
| author_sort |
baker, david |
| spelling |
Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra 2328-9503 2328-9503 Wiley Neurology (clinical) General Neuroscience http://dx.doi.org/10.1002/acn3.792 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Despite progress in treating relapsing multiple sclerosis (<jats:styled-content style="fixed-case">MS</jats:styled-content>), effective inhibition of nonrelapsing progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> is an urgent, unmet, clinical need. Animal models of <jats:styled-content style="fixed-case">MS</jats:styled-content>, such as experimental autoimmune encephalomyelitis (<jats:styled-content style="fixed-case">EAE</jats:styled-content>), provide valuable tools to examine the mechanisms contributing to disease and may be important for developing rational therapeutic approaches for treatment of progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. It has been suggested that myelin oligodendrocyte glycoprotein (<jats:styled-content style="fixed-case">MOG</jats:styled-content>) peptide residues 35‐55 (<jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>)‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in nonobese diabetic (<jats:styled-content style="fixed-case">NOD</jats:styled-content>) mice resembles secondary progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. The objective was to determine whether the published data merits such claims.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Induction and monitoring of EAE in NOD mice and literature review.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>It is evident that the <jats:styled-content style="fixed-case">NOD</jats:styled-content> mouse model lacks validity as a progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> model as the individual course seems to be an asynchronous, relapsing‐remitting neurodegenerative disease, characterized by increasingly poor recovery from relapse. The seemingly progressive course seen in group means of clinical score is an artifact of data handling and interpretation<jats:bold>.</jats:bold></jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>Although <jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in <jats:styled-content style="fixed-case">NOD</jats:styled-content> mice may provide some clues about approaches to block neurodegeneration associated with the inflammatory penumbra as lesions form, it should not be used to justify trials in people with nonactive, progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. This adds further support to the view that drug studies in animals should universally adopt transparent raw data deposition as part of the publication process, such that claims can adequately be interrogated. This transparency is important if animal‐based science is to remain a credible part of translational research in <jats:styled-content style="fixed-case">MS</jats:styled-content>.</jats:p></jats:sec> Autoimmune encephalomyelitis in <scp>NOD</scp> mice is not initially a progressive multiple sclerosis model Annals of Clinical and Translational Neurology |
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2019 |
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Wiley |
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Annals of Clinical and Translational Neurology |
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| title |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_unstemmed |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_full |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_fullStr |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_full_unstemmed |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_short |
Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_sort |
autoimmune encephalomyelitis in <scp>nod</scp> mice is not initially a progressive multiple sclerosis model |
| topic |
Neurology (clinical) General Neuroscience |
| url |
http://dx.doi.org/10.1002/acn3.792 |
| publishDate |
2019 |
| physical |
1362-1372 |
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Despite progress in treating relapsing multiple sclerosis (<jats:styled-content style="fixed-case">MS</jats:styled-content>), effective inhibition of nonrelapsing progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> is an urgent, unmet, clinical need. Animal models of <jats:styled-content style="fixed-case">MS</jats:styled-content>, such as experimental autoimmune encephalomyelitis (<jats:styled-content style="fixed-case">EAE</jats:styled-content>), provide valuable tools to examine the mechanisms contributing to disease and may be important for developing rational therapeutic approaches for treatment of progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. It has been suggested that myelin oligodendrocyte glycoprotein (<jats:styled-content style="fixed-case">MOG</jats:styled-content>) peptide residues 35‐55 (<jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>)‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in nonobese diabetic (<jats:styled-content style="fixed-case">NOD</jats:styled-content>) mice resembles secondary progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. The objective was to determine whether the published data merits such claims.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Induction and monitoring of EAE in NOD mice and literature review.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>It is evident that the <jats:styled-content style="fixed-case">NOD</jats:styled-content> mouse model lacks validity as a progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> model as the individual course seems to be an asynchronous, relapsing‐remitting neurodegenerative disease, characterized by increasingly poor recovery from relapse. The seemingly progressive course seen in group means of clinical score is an artifact of data handling and interpretation<jats:bold>.</jats:bold></jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>Although <jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in <jats:styled-content style="fixed-case">NOD</jats:styled-content> mice may provide some clues about approaches to block neurodegeneration associated with the inflammatory penumbra as lesions form, it should not be used to justify trials in people with nonactive, progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. This adds further support to the view that drug studies in animals should universally adopt transparent raw data deposition as part of the publication process, such that claims can adequately be interrogated. This transparency is important if animal‐based science is to remain a credible part of translational research in <jats:styled-content style="fixed-case">MS</jats:styled-content>.</jats:p></jats:sec> |
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| author | Baker, David, Nutma, Erik, O'Shea, Helen, Cooke, Anne, Orian, Jacqueline M., Amor, Sandra |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Despite progress in treating relapsing multiple sclerosis (<jats:styled-content style="fixed-case">MS</jats:styled-content>), effective inhibition of nonrelapsing progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> is an urgent, unmet, clinical need. Animal models of <jats:styled-content style="fixed-case">MS</jats:styled-content>, such as experimental autoimmune encephalomyelitis (<jats:styled-content style="fixed-case">EAE</jats:styled-content>), provide valuable tools to examine the mechanisms contributing to disease and may be important for developing rational therapeutic approaches for treatment of progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. It has been suggested that myelin oligodendrocyte glycoprotein (<jats:styled-content style="fixed-case">MOG</jats:styled-content>) peptide residues 35‐55 (<jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>)‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in nonobese diabetic (<jats:styled-content style="fixed-case">NOD</jats:styled-content>) mice resembles secondary progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. The objective was to determine whether the published data merits such claims.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Induction and monitoring of EAE in NOD mice and literature review.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>It is evident that the <jats:styled-content style="fixed-case">NOD</jats:styled-content> mouse model lacks validity as a progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> model as the individual course seems to be an asynchronous, relapsing‐remitting neurodegenerative disease, characterized by increasingly poor recovery from relapse. The seemingly progressive course seen in group means of clinical score is an artifact of data handling and interpretation<jats:bold>.</jats:bold></jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>Although <jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in <jats:styled-content style="fixed-case">NOD</jats:styled-content> mice may provide some clues about approaches to block neurodegeneration associated with the inflammatory penumbra as lesions form, it should not be used to justify trials in people with nonactive, progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. This adds further support to the view that drug studies in animals should universally adopt transparent raw data deposition as part of the publication process, such that claims can adequately be interrogated. This transparency is important if animal‐based science is to remain a credible part of translational research in <jats:styled-content style="fixed-case">MS</jats:styled-content>.</jats:p></jats:sec> |
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| spelling | Baker, David Nutma, Erik O'Shea, Helen Cooke, Anne Orian, Jacqueline M. Amor, Sandra 2328-9503 2328-9503 Wiley Neurology (clinical) General Neuroscience http://dx.doi.org/10.1002/acn3.792 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>Despite progress in treating relapsing multiple sclerosis (<jats:styled-content style="fixed-case">MS</jats:styled-content>), effective inhibition of nonrelapsing progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> is an urgent, unmet, clinical need. Animal models of <jats:styled-content style="fixed-case">MS</jats:styled-content>, such as experimental autoimmune encephalomyelitis (<jats:styled-content style="fixed-case">EAE</jats:styled-content>), provide valuable tools to examine the mechanisms contributing to disease and may be important for developing rational therapeutic approaches for treatment of progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. It has been suggested that myelin oligodendrocyte glycoprotein (<jats:styled-content style="fixed-case">MOG</jats:styled-content>) peptide residues 35‐55 (<jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>)‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in nonobese diabetic (<jats:styled-content style="fixed-case">NOD</jats:styled-content>) mice resembles secondary progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. The objective was to determine whether the published data merits such claims.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Induction and monitoring of EAE in NOD mice and literature review.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>It is evident that the <jats:styled-content style="fixed-case">NOD</jats:styled-content> mouse model lacks validity as a progressive <jats:styled-content style="fixed-case">MS</jats:styled-content> model as the individual course seems to be an asynchronous, relapsing‐remitting neurodegenerative disease, characterized by increasingly poor recovery from relapse. The seemingly progressive course seen in group means of clinical score is an artifact of data handling and interpretation<jats:bold>.</jats:bold></jats:p></jats:sec><jats:sec><jats:title>Interpretation</jats:title><jats:p>Although <jats:styled-content style="fixed-case">MOG</jats:styled-content><jats:sup>35‐55</jats:sup>‐induced <jats:styled-content style="fixed-case">EAE</jats:styled-content> in <jats:styled-content style="fixed-case">NOD</jats:styled-content> mice may provide some clues about approaches to block neurodegeneration associated with the inflammatory penumbra as lesions form, it should not be used to justify trials in people with nonactive, progressive <jats:styled-content style="fixed-case">MS</jats:styled-content>. This adds further support to the view that drug studies in animals should universally adopt transparent raw data deposition as part of the publication process, such that claims can adequately be interrogated. This transparency is important if animal‐based science is to remain a credible part of translational research in <jats:styled-content style="fixed-case">MS</jats:styled-content>.</jats:p></jats:sec> Autoimmune encephalomyelitis in <scp>NOD</scp> mice is not initially a progressive multiple sclerosis model Annals of Clinical and Translational Neurology |
| spellingShingle | Baker, David, Nutma, Erik, O'Shea, Helen, Cooke, Anne, Orian, Jacqueline M., Amor, Sandra, Annals of Clinical and Translational Neurology, Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model, Neurology (clinical), General Neuroscience |
| title | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_full | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_fullStr | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_full_unstemmed | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_short | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| title_sort | autoimmune encephalomyelitis in <scp>nod</scp> mice is not initially a progressive multiple sclerosis model |
| title_unstemmed | Autoimmune encephalomyelitis in NOD mice is not initially a progressive multiple sclerosis model |
| topic | Neurology (clinical), General Neuroscience |
| url | http://dx.doi.org/10.1002/acn3.792 |