Lentiviral vector delivery of parkin prevents dopaminergic degeneration in an α-synuclein rat model of Parkinson's disease
Identifieur interne : 000921 ( Pmc/Checkpoint ); précédent : 000920; suivant : 000922Lentiviral vector delivery of parkin prevents dopaminergic degeneration in an α-synuclein rat model of Parkinson's disease
Auteurs : Christophe Lo Bianco [Suisse] ; Bernard L. Schneider [Suisse] ; Matthias Bauer [Suisse] ; Ali Sajadi [Suisse] ; Alexis Brice [France] ; Takeshi Iwatsubo [Japon] ; Patrick Aebischer [Suisse]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2004.
Abstract
Parkinson's disease (PD) is characterized by a progressive loss of midbrain dopamine neurons and the presence of cytoplasmic inclusions called Lewy bodies. Mutations in several genes including α-synuclein and parkin have been linked to familial PD. The loss of parkin's E3-ligase activity leads to dopaminergic neuronal degeneration in early-onset autosomal recessive juvenile parkinsonism, suggesting a key role of parkin for dopamine neuron survival. To evaluate the potential neuroprotective role of parkin in the pathogenesis of PD, we tested whether overexpression of wild-type rat parkin could protect against the toxicity of mutated human A30P α-synuclein in a rat lentiviral model of PD. Animals overexpressing parkin showed significant reductions in α-synuclein-induced neuropathology, including preservation of tyrosine hydroxylase-positive cell bodies in the substantia nigra and sparing of tyrosine hydroxylase-positive nerve terminals in the striatum. The parkin-mediated neuroprotection was associated with an increase in hyperphosphorylated α-synuclein inclusions, suggesting a key role for parkin in the genesis of Lewy bodies. These results indicate that parkin gene therapy may represent a promising candidate treatment for PD.
Url:
DOI: 10.1073/pnas.0405313101
PubMed: 15576511
PubMed Central: 536019
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Parkinson's disease (PD) is characterized by a progressive loss of midbrain dopamine neurons and the presence of cytoplasmic inclusions called Lewy bodies. Mutations in several genes including α-synuclein and parkin have been linked to familial PD. The loss of parkin's E3-ligase activity leads to dopaminergic neuronal degeneration in early-onset autosomal recessive juvenile parkinsonism, suggesting a key role of parkin for dopamine neuron survival. To evaluate the potential neuroprotective role of parkin in the pathogenesis of PD, we tested whether overexpression of wild-type rat parkin could protect against the toxicity of mutated human A30P α-synuclein in a rat lentiviral model of PD. Animals overexpressing parkin showed significant reductions in α-synuclein-induced neuropathology, including preservation of tyrosine hydroxylase-positive cell bodies in the substantia nigra and sparing of tyrosine hydroxylase-positive nerve terminals in the striatum. The parkin-mediated neuroprotection was associated with an increase in hyperphosphorylated α-synuclein inclusions, suggesting a key role for parkin in the genesis of Lewy bodies. These results indicate that parkin gene therapy may represent a promising candidate treatment for PD.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id>
<journal-id journal-id-type="publisher-id">pnas</journal-id>
<journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title>
<issn pub-type="ppub">0027-8424</issn>
<issn pub-type="epub">1091-6490</issn>
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<article-id pub-id-type="doi">10.1073/pnas.0405313101</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject>
<subj-group><subject>Neuroscience</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Lentiviral vector delivery of parkin prevents dopaminergic degeneration in an α-synuclein rat model of Parkinson's disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Lo Bianco</surname>
<given-names>Christophe</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Schneider</surname>
<given-names>Bernard L.</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">*</xref>
<xref ref-type="fn" rid="fn1">†</xref>
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<contrib contrib-type="author"><name><surname>Bauer</surname>
<given-names>Matthias</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sajadi</surname>
<given-names>Ali</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Brice</surname>
<given-names>Alexis</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">‡</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Iwatsubo</surname>
<given-names>Takeshi</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Aebischer</surname>
<given-names>Patrick</given-names>
</name>
<xref ref-type="aff" rid="N0x96db120.0x9cedd28">*</xref>
<xref ref-type="corresp" rid="cor1">¶</xref>
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<aff id="N0x96db120.0x9cedd28"><label>*</label>
Institute of Neuroscience, Swiss Federal Institute of Technology Lausanne, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland;<label>‡</label>
Institut National de la Santé et de la Recherche Médicale U289, Hôpital de la Salpétrière, 75651 Paris, France; and<label>§</label>
Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan</aff>
<author-notes><fn id="cor1"><label>¶</label>
<p> To whom correspondence should be addressed at: Institute of Neuroscience, SG-AAB 132, Swiss Federal institute of Technology Lausanne, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland. E-mail: <email>patrick.aebischer@epfl.ch</email>
. </p>
</fn>
<fn id="fn1"><label>†</label>
<p>Present address: Waisman Center, University of Wisconsin, Madison, WI 53705.</p>
</fn>
<fn><p>Edited by Fred H. Gage, The Salk Institute for Biological Studies, San Diego, CA, and approved October 29, 2004</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><day>14</day>
<month>12</month>
<year>2004</year>
</pub-date>
<pub-date pub-type="epub"><day>2</day>
<month>12</month>
<year>2004</year>
</pub-date>
<volume>101</volume>
<issue>50</issue>
<fpage>17510</fpage>
<lpage>17515</lpage>
<history><date date-type="received"><day>22</day>
<month>7</month>
<year>2004</year>
</date>
</history>
<copyright-statement>Copyright © 2004, The National Academy of Sciences</copyright-statement>
<copyright-year>2004</copyright-year>
<abstract><p>Parkinson's disease (PD) is characterized by a progressive loss of midbrain dopamine neurons and the presence of cytoplasmic inclusions called Lewy bodies. Mutations in several genes including α-synuclein and parkin have been linked to familial PD. The loss of parkin's E3-ligase activity leads to dopaminergic neuronal degeneration in early-onset autosomal recessive juvenile parkinsonism, suggesting a key role of parkin for dopamine neuron survival. To evaluate the potential neuroprotective role of parkin in the pathogenesis of PD, we tested whether overexpression of wild-type rat parkin could protect against the toxicity of mutated human A30P α-synuclein in a rat lentiviral model of PD. Animals overexpressing parkin showed significant reductions in α-synuclein-induced neuropathology, including preservation of tyrosine hydroxylase-positive cell bodies in the substantia nigra and sparing of tyrosine hydroxylase-positive nerve terminals in the striatum. The parkin-mediated neuroprotection was associated with an increase in hyperphosphorylated α-synuclein inclusions, suggesting a key role for parkin in the genesis of Lewy bodies. These results indicate that parkin gene therapy may represent a promising candidate treatment for PD.</p>
</abstract>
<kwd-group><kwd>gene therapy</kwd>
<kwd>lentivirus</kwd>
<kwd>neurodegenerative disease</kwd>
<kwd>Lewy body</kwd>
<kwd>neuroprotection</kwd>
</kwd-group>
</article-meta>
<notes><fn-group><fn><p>Author contributions: C.L. and P.A. designed research; C.L., B.L.S., A.B., and T.I. performed research; C.L., B.L.S., M.B., and A.S. analyzed data; and C.L. and P.A. wrote the paper.</p>
</fn>
<fn><p>This paper was submitted directly (Track II) to the PNAS office.</p>
</fn>
<fn><p>Abbreviations: AR-JP, autosomal recessive juvenile parkinsonism; PD, Parkinson's disease; TH, tyrosine hydroxylase; TH-IR, TH-immunoreactive; YFP, yellow fluorescent protein.</p>
</fn>
</fn-group>
</notes>
</front>
</pmc>
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