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Fingolimod: A Disease-Modifier Drug in a Mouse Model of Amyotrophic Lateral Sclerosis
Fingolimod phosphate (FTY720), the first approved oral therapy for multiple sclerosis, primarily acts as an immunomodulator. Its concomitant effects in the central nervous system, however, indicate a potentially broader spectrum of activity in neurodegenerative diseases. In the present study, we inv...
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| Published in: | Neurotherapeutics 2016-10, Vol.13 (4), p.918-927 |
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| creator | Potenza, Rosa Luisa De Simone, Roberta Armida, Monica Mazziotti, Valentina Pèzzola, Antonella Popoli, Patrizia Minghetti, Luisa |
| description | Fingolimod phosphate (FTY720), the first approved oral therapy for multiple sclerosis, primarily acts as an immunomodulator. Its concomitant effects in the central nervous system, however, indicate a potentially broader spectrum of activity in neurodegenerative diseases. In the present study, we investigated the possible effects of fingolimod in a mouse model of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by a strong neuroinflammatory component. Fingolimod (0.1 and 1 mg/kg i.p.) was administered to mSOD1
G93A
mice, a well-characterized mouse model of ALS, starting from the onset of motor symptoms to the end stage of the disease. The drug was able to improve the neurological phenotype (
p
|
| doi_str_mv | 10.1007/s13311-016-0462-2 |
| format | article |
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G93A
mice, a well-characterized mouse model of ALS, starting from the onset of motor symptoms to the end stage of the disease. The drug was able to improve the neurological phenotype (
p
< 0.05) and to extend the survival (
p
< 0.01) of ALS mice. The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (
CD11b
,
Foxp3
,
iNOS
,
Il1β
,
Il10
,
Arg1
, and
Bdnf
) in motor cortex and spinal cord of animals. Our data show, for the first time, that fingolimod is protective in ALS mice and that its beneficial effects are accompanied by a modulation of microglial activation and innate immunity. Considering that the treatment was started in already symptomatic mice, our data strongly support fingolimod as a potential new therapeutic approach to ALS.</description><identifier>ISSN: 1933-7213</identifier><identifier>ISSN: 1878-7479</identifier><identifier>EISSN: 1878-7479</identifier><identifier>DOI: 10.1007/s13311-016-0462-2</identifier><identifier>PMID: 27456702</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - complications ; Amyotrophic Lateral Sclerosis - drug therapy ; Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - pathology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Body Weight - drug effects ; Body Weight - genetics ; Brain - metabolism ; Brain - pathology ; Cytokines - genetics ; Cytokines - metabolism ; Disease ; Disease Models, Animal ; Fingolimod Hydrochloride - pharmacology ; Fingolimod Hydrochloride - therapeutic use ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Genotype & phenotype ; Humans ; Immunosuppressive Agents - pharmacology ; Immunosuppressive Agents - therapeutic use ; Kinases ; Lymphocytes ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Movement Disorders - drug therapy ; Movement Disorders - etiology ; Multiple sclerosis ; Mutation - genetics ; Nervous system ; Neurobiology ; Neurology ; Neurosciences ; Neurosurgery ; Neurotoxicity ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Original ; Original Article ; Spinal cord ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Spinal Cord - pathology ; Superoxide Dismutase - genetics</subject><ispartof>Neurotherapeutics, 2016-10, Vol.13 (4), p.918-927</ispartof><rights>The American Society for Experimental NeuroTherapeutics, Inc. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-6be26a3c2733fbaebab87878d2ff05cab06ff976c4054e157528f827aa5aa8c83</citedby><cites>FETCH-LOGICAL-c503t-6be26a3c2733fbaebab87878d2ff05cab06ff976c4054e157528f827aa5aa8c83</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/PMC5081121/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081121/$$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/27456702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Potenza, Rosa Luisa</creatorcontrib><creatorcontrib>De Simone, Roberta</creatorcontrib><creatorcontrib>Armida, Monica</creatorcontrib><creatorcontrib>Mazziotti, Valentina</creatorcontrib><creatorcontrib>Pèzzola, Antonella</creatorcontrib><creatorcontrib>Popoli, Patrizia</creatorcontrib><creatorcontrib>Minghetti, Luisa</creatorcontrib><title>Fingolimod: A Disease-Modifier Drug in a Mouse Model of Amyotrophic Lateral Sclerosis</title><title>Neurotherapeutics</title><addtitle>Neurotherapeutics</addtitle><addtitle>Neurotherapeutics</addtitle><description>Fingolimod phosphate (FTY720), the first approved oral therapy for multiple sclerosis, primarily acts as an immunomodulator. Its concomitant effects in the central nervous system, however, indicate a potentially broader spectrum of activity in neurodegenerative diseases. In the present study, we investigated the possible effects of fingolimod in a mouse model of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by a strong neuroinflammatory component. Fingolimod (0.1 and 1 mg/kg i.p.) was administered to mSOD1
G93A
mice, a well-characterized mouse model of ALS, starting from the onset of motor symptoms to the end stage of the disease. The drug was able to improve the neurological phenotype (
p
< 0.05) and to extend the survival (
p
< 0.01) of ALS mice. The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (
CD11b
,
Foxp3
,
iNOS
,
Il1β
,
Il10
,
Arg1
, and
Bdnf
) in motor cortex and spinal cord of animals. Our data show, for the first time, that fingolimod is protective in ALS mice and that its beneficial effects are accompanied by a modulation of microglial activation and innate immunity. Considering that the treatment was started in already symptomatic mice, our data strongly support fingolimod as a potential new therapeutic approach to ALS.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - complications</subject><subject>Amyotrophic Lateral Sclerosis - drug therapy</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - pathology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body Weight - drug effects</subject><subject>Body Weight - genetics</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Fingolimod Hydrochloride - pharmacology</subject><subject>Fingolimod Hydrochloride - therapeutic use</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Immunosuppressive Agents - therapeutic use</subject><subject>Kinases</subject><subject>Lymphocytes</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Movement Disorders - drug therapy</subject><subject>Movement Disorders - etiology</subject><subject>Multiple sclerosis</subject><subject>Mutation - genetics</subject><subject>Nervous system</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Neurotoxicity</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Original</subject><subject>Original Article</subject><subject>Spinal cord</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><subject>Superoxide Dismutase - genetics</subject><issn>1933-7213</issn><issn>1878-7479</issn><issn>1878-7479</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkU1rFTEUhoMotr36A9xIwI2baHIy-RgXwqW1KtziQl2HTCa5TZmZXJMZof_eDLeWKghCSALnOe_5eBF6wegbRql6WxjnjBHKJKGNBAKP0CnTShPVqPZx_becEwWMn6CzUm4oFZy3-ik6AdUIqSicou-XcdqnIY6pf4e3-CIWb4snV6mPIfqML_Kyx3HCFl-lpfh6937AKeDteJvmnA7X0eGdnX22A_7qBp9TieUZehLsUPzzu3dT63z4dv6J7L58_Hy-3REnKJ-J7DxIyx0ozkNnfWe72r3SPYRAhbMdlSG0SrqGisYzoQTooEFZK6zVTvMNen_UPSzd6Hvnp7n2YQ45jjbfmmSj-TMyxWuzTz-NoJqxupgNen0nkNOPxZfZjLE4Pwx28nVewzRX0K7nP1CQCjSIpqKv_kJv0pKnuolVkIIEoFApdqRc3VnJPtz3zahZ_TVHf03116z-mjXn5cOB7zN-G1oBOAKlhqa9zw9K_1P1FxrMr8A</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Potenza, Rosa Luisa</creator><creator>De Simone, Roberta</creator><creator>Armida, Monica</creator><creator>Mazziotti, Valentina</creator><creator>Pèzzola, Antonella</creator><creator>Popoli, Patrizia</creator><creator>Minghetti, Luisa</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161001</creationdate><title>Fingolimod: A Disease-Modifier Drug in a Mouse Model of Amyotrophic Lateral Sclerosis</title><author>Potenza, Rosa Luisa ; De Simone, Roberta ; Armida, Monica ; Mazziotti, Valentina ; Pèzzola, Antonella ; Popoli, Patrizia ; Minghetti, Luisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-6be26a3c2733fbaebab87878d2ff05cab06ff976c4054e157528f827aa5aa8c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - complications</topic><topic>Amyotrophic Lateral Sclerosis - drug therapy</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - pathology</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Body Weight - drug effects</topic><topic>Body Weight - genetics</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Fingolimod Hydrochloride - pharmacology</topic><topic>Fingolimod Hydrochloride - therapeutic use</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - genetics</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Immunosuppressive Agents - therapeutic use</topic><topic>Kinases</topic><topic>Lymphocytes</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Movement Disorders - drug therapy</topic><topic>Movement Disorders - etiology</topic><topic>Multiple sclerosis</topic><topic>Mutation - genetics</topic><topic>Nervous system</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Neurotoxicity</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Original</topic><topic>Original Article</topic><topic>Spinal cord</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><topic>Superoxide Dismutase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Potenza, Rosa Luisa</creatorcontrib><creatorcontrib>De Simone, Roberta</creatorcontrib><creatorcontrib>Armida, Monica</creatorcontrib><creatorcontrib>Mazziotti, Valentina</creatorcontrib><creatorcontrib>Pèzzola, Antonella</creatorcontrib><creatorcontrib>Popoli, Patrizia</creatorcontrib><creatorcontrib>Minghetti, Luisa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database (ProQuest)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurotherapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Potenza, Rosa Luisa</au><au>De Simone, Roberta</au><au>Armida, Monica</au><au>Mazziotti, Valentina</au><au>Pèzzola, Antonella</au><au>Popoli, Patrizia</au><au>Minghetti, Luisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fingolimod: A Disease-Modifier Drug in a Mouse Model of Amyotrophic Lateral Sclerosis</atitle><jtitle>Neurotherapeutics</jtitle><stitle>Neurotherapeutics</stitle><addtitle>Neurotherapeutics</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>13</volume><issue>4</issue><spage>918</spage><epage>927</epage><pages>918-927</pages><issn>1933-7213</issn><issn>1878-7479</issn><eissn>1878-7479</eissn><abstract>Fingolimod phosphate (FTY720), the first approved oral therapy for multiple sclerosis, primarily acts as an immunomodulator. Its concomitant effects in the central nervous system, however, indicate a potentially broader spectrum of activity in neurodegenerative diseases. In the present study, we investigated the possible effects of fingolimod in a mouse model of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by a strong neuroinflammatory component. Fingolimod (0.1 and 1 mg/kg i.p.) was administered to mSOD1
G93A
mice, a well-characterized mouse model of ALS, starting from the onset of motor symptoms to the end stage of the disease. The drug was able to improve the neurological phenotype (
p
< 0.05) and to extend the survival (
p
< 0.01) of ALS mice. The beneficial effect of fingolimod administration was associated with a significant modulation of neuroinflammatory and protective genes (
CD11b
,
Foxp3
,
iNOS
,
Il1β
,
Il10
,
Arg1
, and
Bdnf
) in motor cortex and spinal cord of animals. Our data show, for the first time, that fingolimod is protective in ALS mice and that its beneficial effects are accompanied by a modulation of microglial activation and innate immunity. Considering that the treatment was started in already symptomatic mice, our data strongly support fingolimod as a potential new therapeutic approach to ALS.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27456702</pmid><doi>10.1007/s13311-016-0462-2</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Neurotherapeutics, 2016-10, Vol.13 (4), p.918-927 |
| issn | 1933-7213 1878-7479 1878-7479 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5081121 |
| source | ScienceDirect; Springer Nature; PubMed Central |
| subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - complications Amyotrophic Lateral Sclerosis - drug therapy Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - pathology Animals Biomedical and Life Sciences Biomedicine Body Weight - drug effects Body Weight - genetics Brain - metabolism Brain - pathology Cytokines - genetics Cytokines - metabolism Disease Disease Models, Animal Fingolimod Hydrochloride - pharmacology Fingolimod Hydrochloride - therapeutic use Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Genotype & phenotype Humans Immunosuppressive Agents - pharmacology Immunosuppressive Agents - therapeutic use Kinases Lymphocytes Mice Mice, Inbred C57BL Mice, Transgenic Movement Disorders - drug therapy Movement Disorders - etiology Multiple sclerosis Mutation - genetics Nervous system Neurobiology Neurology Neurosciences Neurosurgery Neurotoxicity Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Original Original Article Spinal cord Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord - pathology Superoxide Dismutase - genetics |
| title | Fingolimod: A Disease-Modifier Drug in a Mouse Model of Amyotrophic Lateral Sclerosis |
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