Towards translational therapies for multiple system atrophy
Identifieur interne : 001700 ( Ncbi/Merge ); précédent : 001699; suivant : 001701Towards translational therapies for multiple system atrophy
Auteurs : Daniela Kuzdas-Wood [Autriche] ; Nadia Stefanova [Autriche] ; Kurt A. Jellinger [Autriche] ; Klaus Seppi [Autriche] ; Michael G. Schlossmacher [Canada] ; Werner Poewe [Autriche] ; Gregor K. Wenning [Autriche]Source :
- Progress in Neurobiology [ 0301-0082 ] ; 2014.
Abstract
This review summarizes the progress made in MSA research during the past decade. Pre-motor features have gained relevance as early diagnostic markers. Animal models have been exploited to discover novel interventional targets. Candidate α-synuclein lowering therapies have been explored in preclinical models.
Url:
DOI: 10.1016/j.pneurobio.2014.02.007
PubMed: 24598411
PubMed Central: 4068324
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Jellinger</name><affiliation wicri:level="3"><nlm:aff id="aff0010">Institute of Clinical Neurobiology, Vienna, Austria</nlm:aff><country xml:lang="fr">Autriche</country><wicri:regionArea>Institute of Clinical Neurobiology, Vienna</wicri:regionArea><placeName><settlement type="city">Vienne (Autriche)</settlement><region nuts="2" type="province">Vienne (Autriche)</region></placeName></affiliation></author><author><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name><affiliation wicri:level="1"><nlm:aff id="aff0005">Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria</nlm:aff><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020</wicri:regionArea><wicri:noRegion>Innsbruck 6020</wicri:noRegion></affiliation></author><author><name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G." last="Schlossmacher">Michael G. Schlossmacher</name><affiliation wicri:level="1"><nlm:aff id="aff0015">Divisions of Neuroscience and Neurology, The Ottawa Hospital Research Institute, University of Ottawa, 451 Smyth Road, RGH #1412, Ottawa, ON, K1H 8M5, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Divisions of Neuroscience and Neurology, The Ottawa Hospital Research Institute, University of Ottawa, 451 Smyth Road, RGH #1412, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation wicri:level="1"><nlm:aff id="aff0005">Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria</nlm:aff><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020</wicri:regionArea><wicri:noRegion>Innsbruck 6020</wicri:noRegion><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name><affiliation wicri:level="1"><nlm:aff id="aff0005">Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria</nlm:aff><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020</wicri:regionArea><wicri:noRegion>Innsbruck 6020</wicri:noRegion></affiliation></author></analytic><series><title level="j">Progress in Neurobiology</title><idno type="ISSN">0301-0082</idno><idno type="eISSN">1873-5118</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>Highlights</title><p><list list-type="simple"><list-item id="lsti0005"><label>•</label><p>This review summarizes the progress made in MSA research during the past decade.</p></list-item><list-item id="lsti0010"><label>•</label><p>Pre-motor features have gained relevance as early diagnostic markers.</p></list-item><list-item id="lsti0015"><label>•</label><p>Animal models have been exploited to discover novel interventional targets.</p></list-item><list-item id="lsti0020"><label>•</label><p>Candidate α-synuclein lowering therapies have been explored in preclinical models.</p></list-item></list></p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Abe, H" uniqKey="Abe H">H. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Prog Neurobiol</journal-id><journal-id journal-id-type="iso-abbrev">Prog. Neurobiol</journal-id><journal-title-group><journal-title>Progress in Neurobiology</journal-title></journal-title-group><issn pub-type="ppub">0301-0082</issn><issn pub-type="epub">1873-5118</issn><publisher><publisher-name>Pergamon Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24598411</article-id><article-id pub-id-type="pmc">4068324</article-id><article-id pub-id-type="publisher-id">S0301-0082(14)00031-8</article-id><article-id pub-id-type="doi">10.1016/j.pneurobio.2014.02.007</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Towards translational therapies for multiple system atrophy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kuzdas-Wood</surname><given-names>Daniela</given-names></name><xref rid="aff0005" ref-type="aff">a</xref></contrib><contrib contrib-type="author"><name><surname>Stefanova</surname><given-names>Nadia</given-names></name><xref rid="aff0005" ref-type="aff">a</xref></contrib><contrib contrib-type="author"><name><surname>Jellinger</surname><given-names>Kurt A.</given-names></name><xref rid="aff0010" ref-type="aff">b</xref></contrib><contrib contrib-type="author"><name><surname>Seppi</surname><given-names>Klaus</given-names></name><xref rid="aff0005" ref-type="aff">a</xref></contrib><contrib contrib-type="author"><name><surname>Schlossmacher</surname><given-names>Michael G.</given-names></name><xref rid="aff0015" ref-type="aff">c</xref></contrib><contrib contrib-type="author"><name><surname>Poewe</surname><given-names>Werner</given-names></name><xref rid="aff0005" ref-type="aff">a</xref></contrib><contrib contrib-type="author"><name><surname>Wenning</surname><given-names>Gregor K.</given-names></name><email>gregor.wenning@i-med.ac.at</email><xref rid="aff0005" ref-type="aff">a</xref><xref rid="cor0005" ref-type="corresp">⁎</xref></contrib></contrib-group><aff id="aff0005"><label>a</label>Department of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria</aff><aff id="aff0010"><label>b</label>Institute of Clinical Neurobiology, Vienna, Austria</aff><aff id="aff0015"><label>c</label>Divisions of Neuroscience and Neurology, The Ottawa Hospital Research Institute, University of Ottawa, 451 Smyth Road, RGH #1412, Ottawa, ON, K1H 8M5, Canada</aff><author-notes><corresp id="cor0005"><label>⁎</label>Corresponding author. Tel.: +43 512 504 81811. <email>gregor.wenning@i-med.ac.at</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>1</day><month>7</month><year>2014</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>7</month><year>2014</year></pub-date><volume>118</volume><issue>100</issue><fpage>19</fpage><lpage>35</lpage><history><date date-type="received"><day>2</day><month>7</month><year>2013</year></date><date date-type="rev-recd"><day>7</day><month>2</month><year>2014</year></date><date date-type="accepted"><day>21</day><month>2</month><year>2014</year></date></history><permissions><copyright-statement>© 2014 Published by Elsevier Ltd.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder></copyright-holder></permissions><abstract abstract-type="author-highlights"><title>Highlights</title><p><list list-type="simple"><list-item id="lsti0005"><label>•</label><p>This review summarizes the progress made in MSA research during the past decade.</p></list-item><list-item id="lsti0010"><label>•</label><p>Pre-motor features have gained relevance as early diagnostic markers.</p></list-item><list-item id="lsti0015"><label>•</label><p>Animal models have been exploited to discover novel interventional targets.</p></list-item><list-item id="lsti0020"><label>•</label><p>Candidate α-synuclein lowering therapies have been explored in preclinical models.</p></list-item></list></p></abstract><abstract><p>Multiple system atrophy (MSA) is a fatal adult-onset neurodegenerative disorder of uncertain etiopathogenesis manifesting with autonomic failure, parkinsonism, and ataxia in any combination. The underlying neuropathology affects central autonomic, striatonigral and olivopontocerebellar pathways and it is associated with distinctive glial cytoplasmic inclusions (GCIs, Papp-Lantos bodies) that contain aggregates of α-synuclein. Current treatment options are very limited and mainly focused on symptomatic relief, whereas disease modifying options are lacking. Despite extensive testing, no neuroprotective drug treatment has been identified up to now; however, a neurorestorative approach utilizing autologous mesenchymal stem cells has shown remarkable beneficial effects in the cerebellar variant of MSA. Here, we review the progress made over the last decade in defining pathogenic targets in MSA and summarize insights gained from candidate disease-modifying interventions that have utilized a variety of well-established preclinical MSA models. We also discuss the current limitations that our field faces and suggest solutions for possible approaches in cause-directed therapies of MSA.</p></abstract><kwd-group><title>Abbreviations</title><kwd>MSA, multiple system atrophy</kwd><kwd>MSA-P, parkinsonian variant of MSA</kwd><kwd>MSA-C, cerebellar variant of MSA</kwd><kwd>α-Syn, alpha-synuclein</kwd><kwd>SND, striatonigral degeneration</kwd><kwd>OPCA, olivopontocerebellar atrophy</kwd><kwd>GCI, (oligodendro-)glial cytoplasmic inclusions</kwd><kwd>UMSARS, unified MSA rating scale</kwd><kwd>wt, wild type</kwd><kwd>tg, transgenic</kwd><kwd>PLP, proteolipid protein</kwd><kwd>MBP, myelin basic protein</kwd><kwd>CNP, 2′,3′-cyclic-nucleotide 3′-phosphodiesterase</kwd><kwd>SN, substantia nigra</kwd></kwd-group><kwd-group><title>Keywords</title><kwd>Multiple system atrophy</kwd><kwd>Striatonigral degeneration</kwd><kwd>Olivopontocerebellar atrophy</kwd><kwd>Alpha-synuclein</kwd><kwd>Neurodegeneration</kwd></kwd-group></article-meta></front><floats-group><fig id="fig0005"><label>Fig. 1</label><caption><p>Neuropathology underlying MSA-P, MSA-C and autonomic failure in MSA. Striatonigral degeneration is the underlying pathology of MSA-P, olivopontocerebellar atrophy occurs in MSA-C and degeneration of autonomic brainstem nuclei plays a role for characteristic autonomic failure in MSA patients. SND, striatonigral degeneration; OPCA, olivopontocerebellar atrophy; SCN, suprachiasmatic nucleus; PVN, paraventricular nucleus; LC, locus coeruleus; VML, ventrolateral medulla; DMV, dorsal motor nucleus of the vagus; NA, nucleus ambiguus; IML, intermediolateral column of the thoracic spinal cord; LDT, laterodorsal tegmental nucleus; PPT, pedunculopontine tegmental nucleus; PAG, periaqueductal gray.</p></caption><graphic xlink:href="gr1"></graphic></fig><fig id="fig0010"><label>Fig. 2</label><caption><p>Possible pathological α-Syn-spreading and accumulation mechanism leading to neurodegeneration. (A) Healthy neuron, oligodendrocyte, microglia and astrocyte, p25α mainly located in the myelinating oligodendroglial processes, monomeric α-Syn present in presynaptic nerve terminals. (B) Relocalisation of p25α from the processes to the soma, inclusion formation and swelling of the oligodendroglial soma. (C) Oligomeric α-Syn accumulation in the oligodendroglial cytoplasm, the exact source of α-Syn remains to be investigated. Possible hypotheses include exocytosed α-Syn from neurons and uptake into oligodendrocytes by cell-to-cell propagation or upregulation of α-Syn expression in oligodendrocytes themselves. In addition, axonal α-Syn may be taken up by the dysfunctional oligodendroglial myelin compartment. (D) α-Syn aggregates form insoluble half-moon shaped GCIs characteristic for the disease. (E) Disruption of trophic support (<italic>e.g.</italic> GDNF), mitochondrial failure, increased production of reactive oxygen species (ROS) and proteasomal dysfunction occur. (F) Oligodendrocytes suffer from severe distress and will eventually degrade. (G) Activation of micro/astroglial cells by cytokines released from the damaged oligodendrocytes, proposed secondary neuronal loss potentially due to lack of trophic support, ROS production, proteasomal failure and pro-inflammatory environment.</p></caption><graphic xlink:href="gr2"></graphic></fig><fig id="fig0015"><label>Fig. 3</label><caption><p>Biomarker-supported early diagnosis of MSA: a pre-requisite for successful trial intervention.</p></caption><graphic xlink:href="gr3"></graphic></fig><table-wrap id="tbl0005" position="float"><label>Table 1</label><caption><p>Overview of characteristic features in human MSA compared to the transgenic models.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left"></th><th align="left">Human</th><th align="left">PLP-α-Syn mouse</th><th align="left">CNP-α-Syn mouse</th><th align="left">MBP-α-Syn mouse</th></tr></thead><tbody><tr><td colspan="5" align="left">Glial pathology</td></tr><tr><td align="left">GCI formation</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td></tr><tr><td align="left">Microgliosis</td><td align="left">✓</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Astrogliosis</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td></tr><tr><td colspan="5" align="left">Neuronal pathology</td></tr><tr><td align="left">SND</td><td align="left">✓</td><td align="left">Degeneration of SNpc and striatum</td><td align="left">n.r.</td><td align="left">Degeneration of dopaminergic nerve terminals in the striatum</td></tr><tr><td align="left">OPCA</td><td align="left">✓</td><td align="left">OPCA-like pathology only after 3-NP challenge</td><td align="left">n.r.</td><td align="left">Neuropathological alterations in the cerebellum</td></tr><tr><td align="left">Central autonomic degeneration</td><td align="left">✓</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Motor impairment</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td><td align="left">✓</td></tr><tr><td colspan="5" align="left">Non-motor features</td></tr><tr><td align="left">Urological disturbances</td><td align="left">✓</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Cardiovascular disturbances</td><td align="left">✓</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Anhidrosis</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Respiratory disturbances</td><td align="left">✓</td><td align="left">n.r.</td><td align="left">n.r.</td><td align="left">n.r.</td></tr><tr><td align="left">Olfactory disturbances</td><td align="left">–</td><td align="left">–</td><td align="left">n.r.</td><td align="left">✓</td></tr><tr><td align="left">References</td><td align="left"><xref rid="bib0050" ref-type="bibr">Benarroch, 2002</xref>, <xref rid="bib0290" ref-type="bibr">Jecmenica-Lukic et al., 2012</xref>, <xref rid="bib0810" ref-type="bibr">Stefanova et al., 2009a</xref>, <xref rid="bib1025" ref-type="bibr">Wenning and Stefanova, 2009</xref>, <xref rid="bib1030" ref-type="bibr">Wenning et al., 2013</xref></td><td align="left"><xref rid="bib0085" ref-type="bibr">Boudes et al., 2013</xref>, <xref rid="bib0320" ref-type="bibr">Kahle et al., 2002</xref>, <xref rid="bib0390" ref-type="bibr">Krismer et al., 2013</xref>, <xref rid="bib0400" ref-type="bibr">Kuzdas et al., 2013</xref>, <xref rid="bib0795" ref-type="bibr">Stefanova et al., 2005, 2008, 2009b, 2012</xref>, <xref rid="bib0840" ref-type="bibr">Stemberger et al. (2010, 2011a)</xref> (<xref rid="bib0180" ref-type="bibr">Flabeau et al., 2014</xref>)</td><td align="left"><xref rid="bib0570 bib0575" ref-type="bibr">Nakayama et al., 2009, 2012</xref>, <xref rid="bib1075" ref-type="bibr">Yazawa et al., 2005</xref></td><td align="left"><xref rid="bib0765" ref-type="bibr">Shults et al., 2005</xref>, <xref rid="bib0905 bib0910 bib0920 bib0930" ref-type="bibr">Ubhi et al., 2008, 2009, 2010b, 2012</xref></td></tr></tbody></table><table-wrap-foot><fn><p>✓, present; –, not present; n.r., not reported.</p></fn></table-wrap-foot></table-wrap><table-wrap id="tbl0010" position="float"><label>Table 2</label><caption><p>Preclinical trials in MSA models.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Intervention</th><th align="left">Animal model</th><th align="left">Results</th></tr></thead><tbody><tr><td align="left" rowspan="2">Riluzole (anti-glutamatergic drug)</td><td align="left">Sequential double-toxin, double-lesion rat model (<xref rid="bib0740" ref-type="bibr">Scherfler et al., 2005</xref>)</td><td align="left">Reduction of motor disturbances, reduction of the striatal lesion volume in the riluzole treated group compared to controls</td></tr><tr><td align="left">MPTP + 3-NP mouse model (<xref rid="bib0125" ref-type="bibr">Diguet et al., 2005</xref>)</td><td align="left">Riluzole improved motor scores and decreased neurodegeneration of striatal neurons</td></tr><tr><td align="left" rowspan="2">Minocycline (tetracycline derivative)</td><td align="left">Double-toxin, double-lesion rat model of MSA (<xref rid="bib0790" ref-type="bibr">Stefanova et al., 2004</xref>)</td><td align="left">No behavioral effects, no neuronal protection, reduced microglial and astroglial activation</td></tr><tr><td align="left">PLP-α-Syn mouse model of MSA (<xref rid="bib0800" ref-type="bibr">Stefanova et al., 2007</xref>)</td><td align="left">Significant reduction of neurodegeneration in the SNpc and striatum</td></tr><tr><td align="left">Rasagiline (irreversible MAO-B inhibitor)</td><td align="left">PLP-α-Syn mouse model of MSA combined with 3-NP administration (<xref rid="bib0805" ref-type="bibr">Stefanova et al., 2008</xref>)</td><td align="left">Behavioral effects, relative preservation of olivopontocerebellar and striatonigral pathways</td></tr><tr><td align="left">Rifampicin (antibiotic)</td><td align="left">MBP-α-Syn mouse model (<xref rid="bib0765 bib0905" ref-type="bibr">Shults et al., 2005; Ubhi et al., 2008</xref>)</td><td align="left">Reduction of α-Syn aggregation</td></tr><tr><td align="left">Nocodazole (microtubule-depolymerizing agent)</td><td align="left">CNP-α-Syn mouse model of MSA (<xref rid="bib0570" ref-type="bibr">Nakayama et al., 2009</xref>)</td><td align="left">Identified β-III-tubulin as key factor in α-Syn-aggregation, administration of nocodazole inhibited the aggregation of soluble α-Syn fibrils, but did not dissolve already formed aggregates</td></tr><tr><td align="left">Terazosin (α1-AR antagonist)</td><td align="left">α1B-Adrenergic receptor overexpressing transgenic MSA mouse model (<xref rid="bib0635 bib1080" ref-type="bibr">Papay et al., 2002; Zuscik et al., 2000</xref>)</td><td align="left">Long-term treatment improved motor deficits and reduced α-Syn-aggregation</td></tr><tr><td align="left">Myeloperoxidase inhibitor (MPO)</td><td align="left">PLP-α-Syn mouse model of MSA combined with 3-NP administration (<xref rid="bib0825" ref-type="bibr">Stefanova et al., 2012</xref>)</td><td align="left">Reduced motor impairment, reduction of intracellular α-Syn aggregates, suppression of microglial activation, reduced degeneration in the striatum, SNpc, Purkinje cells, pontine nuclei and inferior olivary complex</td></tr><tr><td align="left">Fluoxetine (selective serotonin reuptake inhibitor)</td><td align="left">MBP-α-Syn mouse model of MSA (<xref rid="bib0930" ref-type="bibr">Ubhi et al., 2012</xref>)</td><td align="left">Amelioration of motor behavior, reduction of α-Syn aggregation, astrogliosis and demyelination, increased GDNF and BDNF levels, neuroprotection in the frontal cortex, hippocampus and basal ganglia</td></tr><tr><td align="left">Fluoxetine</td><td align="left" rowspan="3">MBP-α-Syn mouse model of MSA (<xref rid="bib0940" ref-type="bibr">Valera et al., 2013</xref>)</td><td align="left" rowspan="3">Reduction of α-Syn aggregation in the basal ganglia, reduced astrogliosis in basal ganglia and hippocampus, modulation of proinflammatory and anti-inflammatory cytokines</td></tr><tr><td align="left">Olanzapine</td></tr><tr><td align="left">Amitriptyline</td></tr><tr><td align="left" rowspan="2">Mesenchymal stem cells</td><td align="left">PLP-α-Syn mouse model of MSA (<xref rid="bib0840" ref-type="bibr">Stemberger et al., 2011a</xref>)</td><td align="left">Relative preservation of SN TH-positive neurons, downregulation of the T-cell specific cytokines IL-2 and IL-17</td></tr><tr><td align="left">MPTP-3-NP double-toxin mouse model (<xref rid="bib0650" ref-type="bibr">Park et al., 2011</xref>)</td><td align="left">Increased survival of dopaminergic neurons in the SN and striatum, anti-inflammatory and anti-gliotic effects</td></tr></tbody></table></table-wrap><table-wrap id="tbl0015" position="float"><label>Table 3</label><caption><p>Clinical trials of MSA.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left"></th><th align="left">Intervention</th><th align="left">Status</th><th align="left">ClinicalTrials.gov identifier</th><th align="left">Study design</th><th align="left">No. of participants</th><th align="left">Main outcome measure</th><th align="left">Results</th></tr></thead><tbody><tr><td align="left" rowspan="8">Completed</td><td align="left">r-hGH (recombinant human growth hormone) (<xref rid="bib0265" ref-type="bibr">Holmberg et al., 2007</xref>)</td><td align="left">Compl.</td><td align="left"></td><td align="left">Phase II randomized, placebo-controlled</td><td align="left">22 treated, 21 placebo</td><td align="left">Safety, UPDRS, UMSARS, CAFTs</td><td align="left">Trend to less worsening in UPDRS, UMSARS and CAFTs suggesting possibility of disease modification; higher dose and/or larger study group (>90) trials recommended</td></tr><tr><td align="left">Riluzole (NNIPPS) (<xref rid="bib0065" ref-type="bibr">Bensimon et al., 2009</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00211224" id="intr0005">NCT00211224</ext-link></td><td align="left">Phase II/III; randomized, placebo-controlled</td><td align="left">194 treated, 197 placebo</td><td align="left">Survival, mortality, different scales (<italic>e.g.</italic> UPDRS, NNIPPS-PPS)</td><td align="left">No evidence of beneficial effect on survival and scales</td></tr><tr><td align="left">Minocycline (MEMSA) (<xref rid="bib0135" ref-type="bibr">Dodel et al., 2010</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00146809" id="intr0010">NCT00146809</ext-link></td><td align="left">Phase II randomized, placebo-controlled</td><td align="left">31 treated, 31 placebo</td><td align="left">UMSARS, UPDRS</td><td align="left">No significant difference between treatment groups</td></tr><tr><td align="left">Rasagiline (<xref rid="bib0670" ref-type="bibr">Poewe et al., 2012</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00977665" id="intr0015">NCT00977665</ext-link></td><td align="left">Phase II; randomized, placebo-controlled</td><td align="left">84 treated, 90 placebo</td><td align="left">UMSARS DWI</td><td align="left">No significant difference between treatment groups on the primary and secondary endpoints</td></tr><tr><td align="left">Lithium carbonate (<xref rid="bib0720" ref-type="bibr">Sacca et al., 2013</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00997672" id="intr0020">NCT00997672</ext-link></td><td align="left">Phase II randomized, placebo-controlled</td><td align="left">4 treated, 5 placebo</td><td align="left">Safety, UMSARS, micro- and macrostructural MR parameters</td><td align="left">Terminated because of side effects</td></tr><tr><td align="left">IVIG (intravenous immunoglobulin) (<xref rid="bib0600" ref-type="bibr">Novak et al., 2012</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00750867" id="intr0025">NCT00750867</ext-link></td><td align="left">Phase II Open label</td><td align="left">7 treated</td><td align="left">Safety, efficacy</td><td align="left">Safe, improved UMSARS scores</td></tr><tr><td align="left">Autologous mesenchymal stem cells (<xref rid="bib0435" ref-type="bibr">Lee et al., 2008b</xref>)</td><td align="left">Compl.</td><td align="left">Not listed</td><td align="left">Phase I/II Open label</td><td align="left">11 treated, 18 historical control group</td><td align="left">Safety, UMSARS, FDG-PET</td><td align="left">Safe, improved UMSARS scores compared to controls, increased FDG-uptake in cerebellum and white matter of the frontal cortex in the in the MSC-treated group compared to baseline<break></break>Increased gray matter density in cerebellum</td></tr><tr><td align="left">Autologous mesenchymal stem cells (<xref rid="bib0430" ref-type="bibr">Lee et al., 2012</xref>)</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT00911365" id="intr0030">NCT00911365</ext-link></td><td align="left">Phase II; randomized placebo-controlled</td><td align="left">14 treated, 17 placebo</td><td align="left">UMSARS</td><td align="left">Delayed progression in UMSARS I and II scores, less extensive decrease in glucose metabolism and gray matter density</td></tr><tr><td colspan="8" align="left">
</td></tr><tr><td align="left" rowspan="2">Pending</td><td align="left">Fluoxetine</td><td align="left">Compl.</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT01146548" id="intr0035">NCT01146548</ext-link></td><td align="left">Phase II randomized, placebo-controlled</td><td align="left"></td><td align="left">UMSARS</td><td align="left">Pending</td></tr><tr><td align="left">Rifampicin</td><td align="left">Ongoing study</td><td align="left"><ext-link ext-link-type="uri" xlink:href="ctgov:NCT01287221" id="intr0040">NCT01287221</ext-link></td><td align="left">Phase II/III; randomized, placebo-controlled</td><td align="left"></td><td align="left">UMSARS</td><td align="left">Pending</td></tr></tbody></table><table-wrap-foot><fn><p>RCT, randomized controlled trial; FDG-PET 0, fluorodeoxyglucose PET; MSC, mesenchymal stem cells; PPS, Parkinson-Plus-Scale; CAFTs, cardiovascular autonomic function tests.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc><affiliations><list><country><li>Autriche</li><li>Canada</li></country><region><li>Tyrol (Land)</li><li>Vienne (Autriche)</li></region><settlement><li>Innsbruck</li><li>Vienne (Autriche)</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="Autriche"><noRegion><name sortKey="Kuzdas Wood, Daniela" sort="Kuzdas Wood, Daniela" uniqKey="Kuzdas Wood D" first="Daniela" last="Kuzdas-Wood">Daniela Kuzdas-Wood</name></noRegion><name sortKey="Jellinger, Kurt A" sort="Jellinger, Kurt A" uniqKey="Jellinger K" first="Kurt A." last="Jellinger">Kurt A. Jellinger</name><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name></country><country name="Canada"><noRegion><name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G." last="Schlossmacher">Michael G. Schlossmacher</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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