Long-term dopamine transporter expression and normal cellular distribution of mitochondria in dopaminergic neuron transplants in Parkinson’s disease patients
Identifieur interne : 000766 ( Pmc/Corpus ); précédent : 000765; suivant : 000767Long-term dopamine transporter expression and normal cellular distribution of mitochondria in dopaminergic neuron transplants in Parkinson’s disease patients
Auteurs : Penelope J. Hallett ; Oliver Cooper ; Damaso Sadi ; Harold Robertson ; Ivar Mendez ; Ole IsacsonSource :
- Cell reports [ 2211-1247 ] ; 2014.
Abstract
To determine the long-term health and function of transplanted dopamine neurons in Parkinson’s disease (PD) patients, the expression of dopamine transporters (DAT) and mitochondrial morphology was examined in human fetal midbrain cellular transplants. DAT was robustly expressed in transplanted dopamine neuron terminals in the reinnervated host putamen and caudate, for at least 14 years after transplantation. The transplanted dopamine neurons showed a healthy and non-atrophied morphology at all time points. Labeling of the mitochondrial outer membrane protein Tom20 and alpha-synuclein showed typical cellular pathology in the patients’ own substantia nigra, which was not observed in transplanted dopamine neurons. These results show that the vast majority of transplanted neurons remain healthy long-term in PD patients, consistent with the clinically maintained function of fetal dopamine neuron transplants for up to 15–18 years in patients. These findings are critically important for the rational development of stem cell-based dopamine neuronal replacement therapies for PD.
Url:
DOI: 10.1016/j.celrep.2014.05.027
PubMed: 24910427
PubMed Central: 4105701
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PMC:4105701Le document en format XML
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Hallett</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author><author><name sortKey="Cooper, Oliver" sort="Cooper, Oliver" uniqKey="Cooper O" first="Oliver" last="Cooper">Oliver Cooper</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author><author><name sortKey="Sadi, Damaso" sort="Sadi, Damaso" uniqKey="Sadi D" first="Damaso" last="Sadi">Damaso Sadi</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Robertson, Harold" sort="Robertson, Harold" uniqKey="Robertson H" first="Harold" last="Robertson">Harold Robertson</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Mendez, Ivar" sort="Mendez, Ivar" uniqKey="Mendez I" first="Ivar" last="Mendez">Ivar Mendez</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Isacson, Ole" sort="Isacson, Ole" uniqKey="Isacson O" first="Ole" last="Isacson">Ole Isacson</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24910427</idno><idno type="pmc">4105701</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105701</idno><idno type="RBID">PMC:4105701</idno><idno type="doi">10.1016/j.celrep.2014.05.027</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000766</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000766</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Long-term dopamine transporter expression and normal cellular distribution of mitochondria in dopaminergic neuron transplants in Parkinson’s disease patients</title><author><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J" last="Hallett">Penelope J. Hallett</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author><author><name sortKey="Cooper, Oliver" sort="Cooper, Oliver" uniqKey="Cooper O" first="Oliver" last="Cooper">Oliver Cooper</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author><author><name sortKey="Sadi, Damaso" sort="Sadi, Damaso" uniqKey="Sadi D" first="Damaso" last="Sadi">Damaso Sadi</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Robertson, Harold" sort="Robertson, Harold" uniqKey="Robertson H" first="Harold" last="Robertson">Harold Robertson</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Mendez, Ivar" sort="Mendez, Ivar" uniqKey="Mendez I" first="Ivar" last="Mendez">Ivar Mendez</name><affiliation><nlm:aff id="A2">Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</nlm:aff></affiliation></author><author><name sortKey="Isacson, Ole" sort="Isacson, Ole" uniqKey="Isacson O" first="Ole" last="Isacson">Ole Isacson</name><affiliation><nlm:aff id="A1">Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Cell reports</title><idno type="eISSN">2211-1247</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Summary</title><p id="P3">To determine the long-term health and function of transplanted dopamine neurons in Parkinson’s disease (PD) patients, the expression of dopamine transporters (DAT) and mitochondrial morphology was examined in human fetal midbrain cellular transplants. DAT was robustly expressed in transplanted dopamine neuron terminals in the reinnervated host putamen and caudate, for at least 14 years after transplantation. The transplanted dopamine neurons showed a healthy and non-atrophied morphology at all time points. Labeling of the mitochondrial outer membrane protein Tom20 and alpha-synuclein showed typical cellular pathology in the patients’ own substantia nigra, which was not observed in transplanted dopamine neurons. These results show that the vast majority of transplanted neurons remain healthy long-term in PD patients, consistent with the clinically maintained function of fetal dopamine neuron transplants for up to 15–18 years in patients. These findings are critically important for the rational development of stem cell-based dopamine neuronal replacement therapies 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>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101573691</journal-id><journal-id journal-id-type="pubmed-jr-id">39703</journal-id><journal-id journal-id-type="nlm-ta">Cell Rep</journal-id><journal-id journal-id-type="iso-abbrev">Cell Rep</journal-id><journal-title-group><journal-title>Cell reports</journal-title></journal-title-group><issn pub-type="epub">2211-1247</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24910427</article-id><article-id pub-id-type="pmc">4105701</article-id><article-id pub-id-type="doi">10.1016/j.celrep.2014.05.027</article-id><article-id pub-id-type="manuscript">NIHMS600456</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Long-term dopamine transporter expression and normal cellular distribution of mitochondria in dopaminergic neuron transplants in Parkinson’s disease patients</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Hallett</surname><given-names>Penelope J</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Cooper</surname><given-names>Oliver</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Sadi</surname><given-names>Damaso</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Robertson</surname><given-names>Harold</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Mendez</surname><given-names>Ivar</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Isacson</surname><given-names>Ole</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>1</label>Harvard University and McLean Hospital, Neuroregeneration Research Institute, 115 Mill Street, Belmont, MA 02478, USA</aff><aff id="A2"><label>2</label>Dalhousie University and Queen Elizabeth II Health Sciences Centre, Division of Neurosurgery and Departments of Anatomy & Neurobiology and Pharmacology, Halifax, Canada B3H 3A7</aff><author-notes><corresp id="FN1"><label>*</label>To whom correspondence should be addressed: Professor Ole, Isacson Neuroregeneration Research Institute, McLean Hospital/Harvard Medical School, MRC 130, 115 Mill St, Belmont MA 02478, <email>isacson@hms.harvard.edu</email>, Tel: (617) 855-3243, Fax: (617) 855-2522</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>10</day><month>6</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>06</day><month>6</month><year>2014</year></pub-date><pub-date pub-type="ppub"><day>26</day><month>6</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>26</day><month>6</month><year>2015</year></pub-date><volume>7</volume><issue>6</issue><fpage>1755</fpage><lpage>1761</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.celrep.2014.05.027</pmc-comment>
<permissions><copyright-statement>© 2014 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year></permissions><abstract><title>Summary</title><p id="P3">To determine the long-term health and function of transplanted dopamine neurons in Parkinson’s disease (PD) patients, the expression of dopamine transporters (DAT) and mitochondrial morphology was examined in human fetal midbrain cellular transplants. DAT was robustly expressed in transplanted dopamine neuron terminals in the reinnervated host putamen and caudate, for at least 14 years after transplantation. The transplanted dopamine neurons showed a healthy and non-atrophied morphology at all time points. Labeling of the mitochondrial outer membrane protein Tom20 and alpha-synuclein showed typical cellular pathology in the patients’ own substantia nigra, which was not observed in transplanted dopamine neurons. These results show that the vast majority of transplanted neurons remain healthy long-term in PD patients, consistent with the clinically maintained function of fetal dopamine neuron transplants for up to 15–18 years in patients. These findings are critically important for the rational development of stem cell-based dopamine neuronal replacement therapies for PD.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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