RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia
The dominant polyglutamine expansion diseases, which include spinocerebellar ataxia type 1 (SCA1) and Huntington disease, are progressive, untreatable, neurodegenerative disorders. In inducible mouse models of SCA1 and Huntington disease, repression of mutant allele expression improves disease pheno...
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| Veröffentlicht in: | Nature medicine 2004-08, Vol.10 (8), p.816-820 |
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| creator | Davidson, Beverly L Xia, Haibin Mao, Qinwen Eliason, Steven L Harper, Scott Q Martins, Inês H Orr, Harry T Paulson, Henry L Yang, Linda Kotin, Robert M |
| description | The dominant polyglutamine expansion diseases, which include spinocerebellar ataxia type 1 (SCA1) and Huntington disease, are progressive, untreatable, neurodegenerative disorders. In inducible mouse models of SCA1 and Huntington disease, repression of mutant allele expression improves disease phenotypes. Thus, therapies designed to inhibit expression of the mutant gene would be beneficial. Here we evaluate the ability of RNA interference (RNAi) to inhibit polyglutamine-induced neurodegeneration caused by mutant ataxin-1 in a mouse model of SCA1. Upon intracerebellar injection, recombinant adeno-associated virus (AAV) vectors expressing short hairpin RNAs profoundly improved motor coordination, restored cerebellar morphology and resolved characteristic ataxin-1 inclusions in Purkinje cells of SCA1 mice. Our data demonstrate
in vivo
the potential use of RNAi as therapy for dominant neurodegenerative disease. |
| doi_str_mv | 10.1038/nm1076 |
| format | Article |
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in vivo
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in vivo
the potential use of RNAi as therapy for dominant neurodegenerative disease.</description><subject>Adeno-associated virus</subject><subject>Adenoviridae</subject><subject>Animals</subject><subject>Ataxin-1</subject><subject>Ataxins</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Northern</subject><subject>Brain - metabolism</subject><subject>Cancer Research</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Gene Expression</subject><subject>Glutamine</subject><subject>Immunohistochemistry</subject><subject>Infectious Diseases</subject><subject>Injection</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Molecular Medicine</subject><subject>Mutants</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - therapy</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nerve Tissue Proteins - pharmacology</subject><subject>Neurosciences</subject><subject>Nuclear Proteins - metabolism</subject><subject>Nuclear Proteins - pharmacology</subject><subject>Plasmids - genetics</subject><subject>Psychomotor Performance - drug effects</subject><subject>Purkinje Cells - drug effects</subject><subject>Purkinje Cells - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference - physiology</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - metabolism</subject><subject>RNA, Small Interfering - therapeutic use</subject><subject>Spinocerebellar Ataxias - pathology</subject><subject>Transduction, Genetic</subject><issn>1078-8956</issn><issn>1546-170X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0t1L3TAUAPAyJtO57S8YI-zBsYe6pGnS9vEi0wmi4D7Yw6Ck6UmNtEnNB-h_v1x6mTovbOQh4eSXQ3JysuwNwYcE0_qTmQiu-LNsj7CS56TCP5-nNa7qvG4Y381een-NMaaYNS-yXcIKylhT72W_Ls9XGvk4zw68B49mO94NYwxi0gZybfoooUcGorM9DGDAiaCtQdoggaYUG5FVyM_aWAkOOhhH4ZAI4laLV9mOEqOH15t5P_t-_Pnb0Zf87OLk9Gh1lkvGi5CrqueclFz1UPVCQsPrkneckgKLplF1moHWRBSlxB2BqmsSUT0uKWBGlKT72cGSd3b2JoIP7aS9XN_EgI2-5bziJefNPyGpMWWkLhJ8_xe8ttGZ9Ii2KCghqYw4oXxBgxih1UbZ4IRcajRaA0qn8Io0tMCc0XXSwy0-jR4mLbce-PjoQDIBbsMgovft6dfL_7cXPx7bgwf2CsQYrrxNn54-1m-F0lnvHah2dnoS7q4luF33Xbv0XYLvNvWK3QT9Pds0WgIfFuDTlhnA3Rf0Saq3izQiRAd_Um22fwPusuYr</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Davidson, Beverly L</creator><creator>Xia, Haibin</creator><creator>Mao, Qinwen</creator><creator>Eliason, Steven L</creator><creator>Harper, Scott Q</creator><creator>Martins, Inês H</creator><creator>Orr, Harry T</creator><creator>Paulson, Henry L</creator><creator>Yang, Linda</creator><creator>Kotin, Robert M</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7QO</scope><scope>7X8</scope></search><sort><creationdate>20040801</creationdate><title>RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia</title><author>Davidson, Beverly L ; Xia, Haibin ; Mao, Qinwen ; Eliason, Steven L ; Harper, Scott Q ; Martins, Inês H ; Orr, Harry T ; Paulson, Henry L ; Yang, Linda ; Kotin, Robert M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-f7d66146fde7dace96846b63120a99f8120e381a24c0b1e7b9e96fd043e051fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adeno-associated virus</topic><topic>Adenoviridae</topic><topic>Animals</topic><topic>Ataxin-1</topic><topic>Ataxins</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Northern</topic><topic>Brain - 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Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davidson, Beverly L</au><au>Xia, Haibin</au><au>Mao, Qinwen</au><au>Eliason, Steven L</au><au>Harper, Scott Q</au><au>Martins, Inês H</au><au>Orr, Harry T</au><au>Paulson, Henry L</au><au>Yang, Linda</au><au>Kotin, Robert M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>10</volume><issue>8</issue><spage>816</spage><epage>820</epage><pages>816-820</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>The dominant polyglutamine expansion diseases, which include spinocerebellar ataxia type 1 (SCA1) and Huntington disease, are progressive, untreatable, neurodegenerative disorders. In inducible mouse models of SCA1 and Huntington disease, repression of mutant allele expression improves disease phenotypes. Thus, therapies designed to inhibit expression of the mutant gene would be beneficial. Here we evaluate the ability of RNA interference (RNAi) to inhibit polyglutamine-induced neurodegeneration caused by mutant ataxin-1 in a mouse model of SCA1. Upon intracerebellar injection, recombinant adeno-associated virus (AAV) vectors expressing short hairpin RNAs profoundly improved motor coordination, restored cerebellar morphology and resolved characteristic ataxin-1 inclusions in Purkinje cells of SCA1 mice. Our data demonstrate
in vivo
the potential use of RNAi as therapy for dominant neurodegenerative disease.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15235598</pmid><doi>10.1038/nm1076</doi><tpages>5</tpages></addata></record> |
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| subjects | Adeno-associated virus Adenoviridae Animals Ataxin-1 Ataxins Biomedical and Life Sciences Biomedicine Blotting, Northern Brain - metabolism Cancer Research Cells, Cultured Disease Models, Animal Gene Expression Glutamine Immunohistochemistry Infectious Diseases Injection Metabolic Diseases Mice Mice, Transgenic Molecular Medicine Mutants Nerve Degeneration - genetics Nerve Degeneration - therapy Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - pharmacology Neurosciences Nuclear Proteins - metabolism Nuclear Proteins - pharmacology Plasmids - genetics Psychomotor Performance - drug effects Purkinje Cells - drug effects Purkinje Cells - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA Interference - physiology RNA, Messenger - metabolism RNA, Small Interfering - metabolism RNA, Small Interfering - therapeutic use Spinocerebellar Ataxias - pathology Transduction, Genetic |
| title | RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia |
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