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Reversal of axonal loss and disability in a mouse model of progressive multiple sclerosis
Axonal degeneration is an important determinant of progressive neurological disability in multiple sclerosis (MS). Thus, therapeutic approaches promoting neuroprotection could aid the treatment of progressive MS. Here, we used what we believe is a novel water-soluble fullerene derivative (ABS-75) at...
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Published in: | The Journal of clinical investigation 2008-04, Vol.118 (4), p.1532-1543 |
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creator | Basso, Alexandre S Frenkel, Dan Quintana, Francisco J Costa-Pinto, Frederico A Petrovic-Stojkovic, Sanja Puckett, Lindsay Monsonego, Alon Bar-Shir, Amnon Engel, Yoni Gozin, Michael Weiner, Howard L |
description | Axonal degeneration is an important determinant of progressive neurological disability in multiple sclerosis (MS). Thus, therapeutic approaches promoting neuroprotection could aid the treatment of progressive MS. Here, we used what we believe is a novel water-soluble fullerene derivative (ABS-75) attached to an NMDA receptor antagonist, which combines antioxidant and anti-excitotoxic properties, to block axonal damage and reduce disease progression in a chronic progressive EAE model. Fullerene ABS-75 treatment initiated after disease onset reduced the clinical progression of chronic EAE in NOD mice immunized with myelin-oligodendrocyte glycoprotein (MOG). Reduced disease progression in ABS-75-treated mice was associated with reduced axonal loss and demyelination in the spinal cord. Fullerene ABS-75 halted oxidative injury, CD11b+ infiltration, and CCL2 expression in the spinal cord of mice without interfering with antigen-specific T cell responses. In vitro, fullerene ABS-75 protected neurons from oxidative and glutamate-induced injury and restored glutamine synthetase and glutamate transporter expression in astrocytes under inflammatory insult. Glutamine synthetase expression was also increased in the white matter of fullerene ABS-75-treated animals. Our data demonstrate the neuroprotective effect of treatment with a fullerene compound combined with a NMDA receptor antagonist, which may be useful in the treatment of progressive MS and other neurodegenerative diseases. |
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Thus, therapeutic approaches promoting neuroprotection could aid the treatment of progressive MS. Here, we used what we believe is a novel water-soluble fullerene derivative (ABS-75) attached to an NMDA receptor antagonist, which combines antioxidant and anti-excitotoxic properties, to block axonal damage and reduce disease progression in a chronic progressive EAE model. Fullerene ABS-75 treatment initiated after disease onset reduced the clinical progression of chronic EAE in NOD mice immunized with myelin-oligodendrocyte glycoprotein (MOG). Reduced disease progression in ABS-75-treated mice was associated with reduced axonal loss and demyelination in the spinal cord. Fullerene ABS-75 halted oxidative injury, CD11b+ infiltration, and CCL2 expression in the spinal cord of mice without interfering with antigen-specific T cell responses. In vitro, fullerene ABS-75 protected neurons from oxidative and glutamate-induced injury and restored glutamine synthetase and glutamate transporter expression in astrocytes under inflammatory insult. Glutamine synthetase expression was also increased in the white matter of fullerene ABS-75-treated animals. Our data demonstrate the neuroprotective effect of treatment with a fullerene compound combined with a NMDA receptor antagonist, which may be useful in the treatment of progressive MS and other neurodegenerative diseases.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/jci33464</identifier><identifier>PMID: 18340379</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Amino Acid Transport System X-AG - metabolism ; Animals ; Antioxidants ; Astrocytes - drug effects ; Astrocytes - metabolism ; Axons - drug effects ; Axons - metabolism ; Axons - pathology ; B-Lymphocytes - drug effects ; Biomedical research ; Blood-brain barrier ; Care and treatment ; CD11b Antigen - metabolism ; Chemokine CCL2 - metabolism ; Chronic Disease ; Complications and side effects ; Disability ; Disease ; Disease Models, Animal ; Disease Progression ; Drug therapy ; Fullerenes ; Fullerenes - chemistry ; Fullerenes - therapeutic use ; Glutamic Acid - pharmacology ; Glycoproteins ; Immunization ; Memory - drug effects ; Mice ; Molecular Structure ; Multiple sclerosis ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - metabolism ; Multiple Sclerosis - pathology ; Oxidative Stress - drug effects ; Peptides ; Risk factors ; Spinal cord ; T-Lymphocytes - drug effects ; Whooping cough</subject><ispartof>The Journal of clinical investigation, 2008-04, Vol.118 (4), p.1532-1543</ispartof><rights>COPYRIGHT 2008 American Society for Clinical Investigation</rights><rights>Copyright American Society for Clinical Investigation Apr 2008</rights><rights>Copyright © 2008, American Society for Clinical Investigation 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c639t-e7659a1a095f45d8288702cc862c0a8be10f24468f2a4f9a8b1977f454fc14613</citedby><cites>FETCH-LOGICAL-c639t-e7659a1a095f45d8288702cc862c0a8be10f24468f2a4f9a8b1977f454fc14613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267014/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267014/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18340379$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Basso, Alexandre S</creatorcontrib><creatorcontrib>Frenkel, Dan</creatorcontrib><creatorcontrib>Quintana, Francisco J</creatorcontrib><creatorcontrib>Costa-Pinto, Frederico A</creatorcontrib><creatorcontrib>Petrovic-Stojkovic, Sanja</creatorcontrib><creatorcontrib>Puckett, Lindsay</creatorcontrib><creatorcontrib>Monsonego, Alon</creatorcontrib><creatorcontrib>Bar-Shir, Amnon</creatorcontrib><creatorcontrib>Engel, Yoni</creatorcontrib><creatorcontrib>Gozin, Michael</creatorcontrib><creatorcontrib>Weiner, Howard L</creatorcontrib><title>Reversal of axonal loss and disability in a mouse model of progressive multiple sclerosis</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Axonal degeneration is an important determinant of progressive neurological disability in multiple sclerosis (MS). Thus, therapeutic approaches promoting neuroprotection could aid the treatment of progressive MS. Here, we used what we believe is a novel water-soluble fullerene derivative (ABS-75) attached to an NMDA receptor antagonist, which combines antioxidant and anti-excitotoxic properties, to block axonal damage and reduce disease progression in a chronic progressive EAE model. Fullerene ABS-75 treatment initiated after disease onset reduced the clinical progression of chronic EAE in NOD mice immunized with myelin-oligodendrocyte glycoprotein (MOG). Reduced disease progression in ABS-75-treated mice was associated with reduced axonal loss and demyelination in the spinal cord. Fullerene ABS-75 halted oxidative injury, CD11b+ infiltration, and CCL2 expression in the spinal cord of mice without interfering with antigen-specific T cell responses. In vitro, fullerene ABS-75 protected neurons from oxidative and glutamate-induced injury and restored glutamine synthetase and glutamate transporter expression in astrocytes under inflammatory insult. Glutamine synthetase expression was also increased in the white matter of fullerene ABS-75-treated animals. Our data demonstrate the neuroprotective effect of treatment with a fullerene compound combined with a NMDA receptor antagonist, which may be useful in the treatment of progressive MS and other neurodegenerative diseases.</description><subject>Amino Acid Transport System X-AG - metabolism</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - metabolism</subject><subject>Axons - drug effects</subject><subject>Axons - metabolism</subject><subject>Axons - pathology</subject><subject>B-Lymphocytes - drug effects</subject><subject>Biomedical research</subject><subject>Blood-brain barrier</subject><subject>Care and treatment</subject><subject>CD11b Antigen - metabolism</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chronic Disease</subject><subject>Complications and side effects</subject><subject>Disability</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Drug therapy</subject><subject>Fullerenes</subject><subject>Fullerenes - 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metabolism</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - metabolism</topic><topic>Axons - drug effects</topic><topic>Axons - metabolism</topic><topic>Axons - pathology</topic><topic>B-Lymphocytes - drug effects</topic><topic>Biomedical research</topic><topic>Blood-brain barrier</topic><topic>Care and treatment</topic><topic>CD11b Antigen - metabolism</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chronic Disease</topic><topic>Complications and side effects</topic><topic>Disability</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Drug therapy</topic><topic>Fullerenes</topic><topic>Fullerenes - chemistry</topic><topic>Fullerenes - therapeutic use</topic><topic>Glutamic Acid - pharmacology</topic><topic>Glycoproteins</topic><topic>Immunization</topic><topic>Memory - drug effects</topic><topic>Mice</topic><topic>Molecular Structure</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - 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Thus, therapeutic approaches promoting neuroprotection could aid the treatment of progressive MS. Here, we used what we believe is a novel water-soluble fullerene derivative (ABS-75) attached to an NMDA receptor antagonist, which combines antioxidant and anti-excitotoxic properties, to block axonal damage and reduce disease progression in a chronic progressive EAE model. Fullerene ABS-75 treatment initiated after disease onset reduced the clinical progression of chronic EAE in NOD mice immunized with myelin-oligodendrocyte glycoprotein (MOG). Reduced disease progression in ABS-75-treated mice was associated with reduced axonal loss and demyelination in the spinal cord. Fullerene ABS-75 halted oxidative injury, CD11b+ infiltration, and CCL2 expression in the spinal cord of mice without interfering with antigen-specific T cell responses. In vitro, fullerene ABS-75 protected neurons from oxidative and glutamate-induced injury and restored glutamine synthetase and glutamate transporter expression in astrocytes under inflammatory insult. Glutamine synthetase expression was also increased in the white matter of fullerene ABS-75-treated animals. Our data demonstrate the neuroprotective effect of treatment with a fullerene compound combined with a NMDA receptor antagonist, which may be useful in the treatment of progressive MS and other neurodegenerative diseases.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>18340379</pmid><doi>10.1172/jci33464</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amino Acid Transport System X-AG - metabolism Animals Antioxidants Astrocytes - drug effects Astrocytes - metabolism Axons - drug effects Axons - metabolism Axons - pathology B-Lymphocytes - drug effects Biomedical research Blood-brain barrier Care and treatment CD11b Antigen - metabolism Chemokine CCL2 - metabolism Chronic Disease Complications and side effects Disability Disease Disease Models, Animal Disease Progression Drug therapy Fullerenes Fullerenes - chemistry Fullerenes - therapeutic use Glutamic Acid - pharmacology Glycoproteins Immunization Memory - drug effects Mice Molecular Structure Multiple sclerosis Multiple Sclerosis - drug therapy Multiple Sclerosis - metabolism Multiple Sclerosis - pathology Oxidative Stress - drug effects Peptides Risk factors Spinal cord T-Lymphocytes - drug effects Whooping cough |
title | Reversal of axonal loss and disability in a mouse model of progressive multiple sclerosis |
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