Targeting chelatable iron as a therapeutic modality in Parkinson's disease.
Identifieur interne : 000535 ( PubMed/Corpus ); précédent : 000534; suivant : 000536Targeting chelatable iron as a therapeutic modality in Parkinson's disease.
Auteurs : David Devos ; Caroline Moreau ; Jean Christophe Devedjian ; Jérome Kluza ; Maud Petrault ; Charlotte Laloux ; Aurélie Jonneaux ; Gilles Ryckewaert ; Guillaume Garçon ; Nathalie Rouaix ; Alain Duhamel ; Patrice Jissendi ; Kathy Dujardin ; Florent Auger ; Laura Ravasi ; Lucie Hopes ; Guillaume Grolez ; Wance Firdaus ; Bernard Sablonnière ; Isabelle Strubi-Vuillaume ; Noel Zahr ; Alain Destée ; Jean-Christophe Corvol ; Dominik Pöltl ; Marcel Leist ; Christian Rose ; Luc Defebvre ; Philippe Marchetti ; Z Ioav Cabantchik ; Régis BordetSource :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Cell Line, Combined Modality Therapy, Disease Models, Animal, Double-Blind Method, Humans, Iron (metabolism), Iron Chelating Agents (administration & dosage), Iron Chelating Agents (therapeutic use), Male, Mice, Mice, Inbred C57BL, Motor Activity (drug effects), Oxidative Stress (drug effects), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Pilot Projects, Pyridones (administration & dosage), Pyridones (pharmacology), Pyridones (therapeutic use).
- MESH :
- chemical , administration & dosage : Iron Chelating Agents, Pyridones.
- chemical , metabolism : Iron.
- chemical , pharmacology : Pyridones.
- chemical , therapeutic use : Iron Chelating Agents, Pyridones.
- drug effects : Motor Activity, Oxidative Stress.
- drug therapy : Parkinson Disease.
- metabolism : Parkinson Disease.
- Animals, Cell Line, Combined Modality Therapy, Disease Models, Animal, Double-Blind Method, Humans, Male, Mice, Mice, Inbred C57BL, Pilot Projects.
Abstract
The pathophysiological role of iron in Parkinson's disease (PD) was assessed by a chelation strategy aimed at reducing oxidative damage associated with regional iron deposition without affecting circulating metals. Translational cell and animal models provided concept proofs and a delayed-start (DS) treatment paradigm, the basis for preliminary clinical assessments.
DOI: 10.1089/ars.2013.5593
PubMed: 24251381
Links to Exploration step
pubmed:24251381Le document en format XML
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<term>Cell Line</term>
<term>Combined Modality Therapy</term>
<term>Disease Models, Animal</term>
<term>Double-Blind Method</term>
<term>Humans</term>
<term>Iron (metabolism)</term>
<term>Iron Chelating Agents (administration & dosage)</term>
<term>Iron Chelating Agents (therapeutic use)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Motor Activity (drug effects)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Pilot Projects</term>
<term>Pyridones (administration & dosage)</term>
<term>Pyridones (pharmacology)</term>
<term>Pyridones (therapeutic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Iron Chelating Agents</term>
<term>Pyridones</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Iron</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Pyridones</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Iron Chelating Agents</term>
<term>Pyridones</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term>
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<term>Cell Line</term>
<term>Combined Modality Therapy</term>
<term>Disease Models, Animal</term>
<term>Double-Blind Method</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Pilot Projects</term>
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<front><div type="abstract" xml:lang="en">The pathophysiological role of iron in Parkinson's disease (PD) was assessed by a chelation strategy aimed at reducing oxidative damage associated with regional iron deposition without affecting circulating metals. Translational cell and animal models provided concept proofs and a delayed-start (DS) treatment paradigm, the basis for preliminary clinical assessments.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24251381</PMID>
<DateCreated><Year>2014</Year>
<Month>06</Month>
<Day>17</Day>
</DateCreated>
<DateCompleted><Year>2015</Year>
<Month>03</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>12</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>21</Volume>
<Issue>2</Issue>
<PubDate><Year>2014</Year>
<Month>Jul</Month>
<Day>10</Day>
</PubDate>
</JournalIssue>
<Title>Antioxidants & redox signaling</Title>
<ISOAbbreviation>Antioxid. Redox Signal.</ISOAbbreviation>
</Journal>
<ArticleTitle>Targeting chelatable iron as a therapeutic modality in Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>195-210</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1089/ars.2013.5593</ELocationID>
<Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">The pathophysiological role of iron in Parkinson's disease (PD) was assessed by a chelation strategy aimed at reducing oxidative damage associated with regional iron deposition without affecting circulating metals. Translational cell and animal models provided concept proofs and a delayed-start (DS) treatment paradigm, the basis for preliminary clinical assessments.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">For translational studies, we assessed the effect of oxidative insults in mice systemically prechelated with deferiprone (DFP) by following motor functions, striatal dopamine (HPLC and MRI-PET), and brain iron deposition (relaxation-R2*-MRI) aided by spectroscopic measurements of neuronal labile iron (with fluorescence-sensitive iron sensors) and oxidative damage by markers of protein, lipid, and DNA modification. DFP significantly reduced labile iron and biological damage in oxidation-stressed cells and animals, improving motor functions while raising striatal dopamine. For a pilot, double-blind, placebo-controlled randomized clinical trial, early-stage Parkinson's patients on stabilized dopamine regimens enrolled in a 12-month single-center study with DFP (30 mg/kg/day). Based on a 6-month DS paradigm, early-start patients (n=19) compared to DS patients (n=18) (37/40 completed) responded significantly earlier and sustainably to treatment in both substantia nigra iron deposits (R2* MRI) and Unified Parkinson's Disease Rating Scale motor indicators of disease progression (p<0.03 and p<0.04, respectively). Apart from three rapidly resolved neutropenia cases, safety was maintained throughout the trial.</AbstractText>
<AbstractText Label="INNOVATION" NlmCategory="METHODS">A moderate iron chelation regimen that avoids changes in systemic iron levels may constitute a novel therapeutic modality for PD.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The therapeutic features of a chelation modality established in translational models and in pilot clinical trials warrant comprehensive evaluation of symptomatic and/or disease-modifying potential of chelation in PD.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Devos</LastName>
<ForeName>David</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>1 Department of Medical Pharmacology, Faculté de Médecine Lille2, Lille Nord de France University , CHU Lille, Lille, France .</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Moreau</LastName>
<ForeName>Caroline</ForeName>
<Initials>C</Initials>
</Author>
<Author ValidYN="Y"><LastName>Devedjian</LastName>
<ForeName>Jean Christophe</ForeName>
<Initials>JC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kluza</LastName>
<ForeName>Jérome</ForeName>
<Initials>J</Initials>
</Author>
<Author ValidYN="Y"><LastName>Petrault</LastName>
<ForeName>Maud</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Laloux</LastName>
<ForeName>Charlotte</ForeName>
<Initials>C</Initials>
</Author>
<Author ValidYN="Y"><LastName>Jonneaux</LastName>
<ForeName>Aurélie</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ryckewaert</LastName>
<ForeName>Gilles</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Garçon</LastName>
<ForeName>Guillaume</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Rouaix</LastName>
<ForeName>Nathalie</ForeName>
<Initials>N</Initials>
</Author>
<Author ValidYN="Y"><LastName>Duhamel</LastName>
<ForeName>Alain</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Jissendi</LastName>
<ForeName>Patrice</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Dujardin</LastName>
<ForeName>Kathy</ForeName>
<Initials>K</Initials>
</Author>
<Author ValidYN="Y"><LastName>Auger</LastName>
<ForeName>Florent</ForeName>
<Initials>F</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ravasi</LastName>
<ForeName>Laura</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Hopes</LastName>
<ForeName>Lucie</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Grolez</LastName>
<ForeName>Guillaume</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Firdaus</LastName>
<ForeName>Wance</ForeName>
<Initials>W</Initials>
</Author>
<Author ValidYN="Y"><LastName>Sablonnière</LastName>
<ForeName>Bernard</ForeName>
<Initials>B</Initials>
</Author>
<Author ValidYN="Y"><LastName>Strubi-Vuillaume</LastName>
<ForeName>Isabelle</ForeName>
<Initials>I</Initials>
</Author>
<Author ValidYN="Y"><LastName>Zahr</LastName>
<ForeName>Noel</ForeName>
<Initials>N</Initials>
</Author>
<Author ValidYN="Y"><LastName>Destée</LastName>
<ForeName>Alain</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Corvol</LastName>
<ForeName>Jean-Christophe</ForeName>
<Initials>JC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Pöltl</LastName>
<ForeName>Dominik</ForeName>
<Initials>D</Initials>
</Author>
<Author ValidYN="Y"><LastName>Leist</LastName>
<ForeName>Marcel</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Rose</LastName>
<ForeName>Christian</ForeName>
<Initials>C</Initials>
</Author>
<Author ValidYN="Y"><LastName>Defebvre</LastName>
<ForeName>Luc</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Marchetti</LastName>
<ForeName>Philippe</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Cabantchik</LastName>
<ForeName>Z Ioav</ForeName>
<Initials>ZI</Initials>
</Author>
<Author ValidYN="Y"><LastName>Bordet</LastName>
<ForeName>Régis</ForeName>
<Initials>R</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName>
<AccessionNumberList><AccessionNumber>NCT00943748</AccessionNumber>
</AccessionNumberList>
</DataBank>
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<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016449">Randomized Controlled Trial</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>02</Month>
<Day>06</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Antioxid Redox Signal</MedlineTA>
<NlmUniqueID>100888899</NlmUniqueID>
<ISSNLinking>1523-0864</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007502">Iron Chelating Agents</NameOfSubstance>
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