Progression of Intestinal Permeability Changes and Alpha-Synuclein Expression in a Mouse Model of Parkinson’s Disease
Identifieur interne : 000826 ( Main/Exploration ); précédent : 000825; suivant : 000827Progression of Intestinal Permeability Changes and Alpha-Synuclein Expression in a Mouse Model of Parkinson’s Disease
Auteurs : Leo P. Kelly [États-Unis] ; Paul M. Carvey [États-Unis] ; Ali Keshavarzian [États-Unis, Pays-Bas] ; Kathleen M. Shannon [États-Unis] ; Maliha Shaikh [États-Unis] ; Roy A. E. Bakay [États-Unis] ; Jeffrey H. Kordower [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Brain (metabolism), Brain (pathology), Chromatography, Gas, Colon (drug effects), Colon (metabolism), Colon (pathology), Disease Models, Animal, Disease Progression, Gastrointestinal Agents (urine), Linear Models, Male, Mice, Mice, Inbred C57BL, Parkinson Disease (etiology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (urine), Permeability (drug effects), Polysaccharides (toxicity), Severity of Illness Index, Time Factors, Tyrosine 3-Monooxygenase (metabolism), Vagus Nerve (metabolism), Vagus Nerve (pathology), alpha-Synuclein (metabolism).
- MESH :
- chemical , metabolism : Tyrosine 3-Monooxygenase, alpha-Synuclein.
- chemical , toxicity : Polysaccharides.
- chemical , urine : Gastrointestinal Agents.
- drug effects : Colon, Permeability.
- etiology : Parkinson Disease.
- metabolism : Brain, Colon, Parkinson Disease, Vagus Nerve.
- pathology : Brain, Colon, Parkinson Disease, Vagus Nerve.
- urine : Parkinson Disease.
- Animals, Chromatography, Gas, Disease Models, Animal, Disease Progression, Linear Models, Male, Mice, Mice, Inbred C57BL, Severity of Illness Index, Time Factors.
Abstract
Parkinson’s disease (PD) is a multifocal degenerative disorder for which there is no cure. The majority of cases are sporadic with unknown etiology. Recent data indicate that untreated patients with de novo PD have increased colonic permeability and that both de novo and premotor patients have pathological expression of α-synuclein (α-syn) in their colon. Both endpoints potentially can serve as disease biomarkers and even may initiate PD events through gut-derived, lipopolysaccharide (LPS)-induced neuronal injury. Animal models could be ideal for interrogating the potential role of the intestines in the pathogenesis of PD; however, few current animal models of PD encompass these nonmotor features. We sought to establish a progressive model of PD that includes the gastrointestinal (GI) dysfunction present in human patients. C57/BL6 mice were systemically administered one dose of either LPS (2.5 mg/kg) or saline and were sacrificed in monthly intervals (n=5 mice for 5 months) to create a time-course. Small and large intestinal permeability was assessed by analyzing the urinary output of orally ingested sugar probes through capillary column gas chromatography. α-Syn expression was assessed by counting the number of mildly, moderately, and severely affected myenteric ganglia neurons throughout the GI tract, and the counts were validated by quantitative optical density measurements. Nigrostriatal integrity was assessed by tyrosine hydroxylase immunohistochemistry stereology and densitometry. LPS caused an immediate and progressive increase in α-syn expression in the large intestine but not in the small intestine. Intestinal permeability of the whole gut (large and small intestines) progressively increased between months 2 and 4 after LPS administration but returned to baseline levels at month 5. Selective measurements demonstrated that intestinal permeability in the small intestine remained largely intact, suggesting that gut leakiness was predominately in the large intestine. Phosphorylated serine 129-α-syn was identified in a subset of colonic myenteric neurons at months 4 and 5. Although these changes were observed in the absence of nigrostriatal degeneration, an abrupt but insignificant increase in brainstem α-syn was observed that paralleled the restoration of permeability. No changes were observed over time in controls. LPS, an endotoxin used to model PD, causes sequential increases in α-syn immunoreactivity, intestinal permeability, and pathological α-syn accumulation in the colon in a manner similar to that observed in patients with PD. These features are observed without nigrostriatal degeneration and incorporate PD features before the motor syndrome. This allows for the potential use of this model in testing neuroprotective and disease-modifying therapies, including intestinal-directed therapies to fortify intestinal barrier integrity.
Url:
DOI: 10.1002/mds.25736
PubMed: 24898698
PubMed Central: 4050039
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000406
- to stream Pmc, to step Curation: 000406
- to stream Pmc, to step Checkpoint: 000085
- to stream PubMed, to step Corpus: 000486
- to stream PubMed, to step Curation: 000486
- to stream PubMed, to step Checkpoint: 000467
- to stream Ncbi, to step Merge: 004013
- to stream Ncbi, to step Curation: 004013
- to stream Ncbi, to step Checkpoint: 004013
- to stream Main, to step Merge: 000826
- to stream Main, to step Curation: 000826
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Progression of Intestinal Permeability Changes and Alpha-Synuclein Expression in a Mouse Model of Parkinson’s Disease</title>
<author><name sortKey="Kelly, Leo P" sort="Kelly, Leo P" uniqKey="Kelly L" first="Leo P." last="Kelly">Leo P. Kelly</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurosurgery, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurosurgery, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M." last="Carvey">Paul M. Carvey</name>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Keshavarzian, Ali" sort="Keshavarzian, Ali" uniqKey="Keshavarzian A" first="Ali" last="Keshavarzian">Ali Keshavarzian</name>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A3">Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="4"><nlm:aff id="A4">Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, the Netherlands</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht</wicri:regionArea>
<placeName><settlement type="city">Utrecht</settlement>
<region nuts="2" type="province">Utrecht (province)</region>
</placeName>
<orgName type="university">Université d'Utrecht</orgName>
</affiliation>
</author>
<author><name sortKey="Shannon, Kathleen M" sort="Shannon, Kathleen M" uniqKey="Shannon K" first="Kathleen M." last="Shannon">Kathleen M. Shannon</name>
<affiliation wicri:level="2"><nlm:aff id="A5">Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Shaikh, Maliha" sort="Shaikh, Maliha" uniqKey="Shaikh M" first="Maliha" last="Shaikh">Maliha Shaikh</name>
<affiliation wicri:level="2"><nlm:aff id="A3">Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurosurgery, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurosurgery, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Kordower, Jeffrey H" sort="Kordower, Jeffrey H" uniqKey="Kordower J" first="Jeffrey H." last="Kordower">Jeffrey H. Kordower</name>
<affiliation wicri:level="2"><nlm:aff id="A5">Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">24898698</idno>
<idno type="pmc">4050039</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050039</idno>
<idno type="RBID">PMC:4050039</idno>
<idno type="doi">10.1002/mds.25736</idno>
<date when="2013">2013</date>
<idno type="wicri:Area/Pmc/Corpus">000406</idno>
<idno type="wicri:Area/Pmc/Curation">000406</idno>
<idno type="wicri:Area/Pmc/Checkpoint">000085</idno>
<idno type="wicri:source">PubMed</idno>
<idno type="wicri:Area/PubMed/Corpus">000486</idno>
<idno type="wicri:Area/PubMed/Curation">000486</idno>
<idno type="wicri:Area/PubMed/Checkpoint">000467</idno>
<idno type="wicri:Area/Ncbi/Merge">004013</idno>
<idno type="wicri:Area/Ncbi/Curation">004013</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">004013</idno>
<idno type="wicri:doubleKey">0885-3185:2013:Kelly L:progression:of:intestinal</idno>
<idno type="wicri:Area/Main/Merge">000826</idno>
<idno type="wicri:Area/Main/Curation">000826</idno>
<idno type="wicri:Area/Main/Exploration">000826</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Progression of Intestinal Permeability Changes and Alpha-Synuclein Expression in a Mouse Model of Parkinson’s Disease</title>
<author><name sortKey="Kelly, Leo P" sort="Kelly, Leo P" uniqKey="Kelly L" first="Leo P." last="Kelly">Leo P. Kelly</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurosurgery, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurosurgery, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M." last="Carvey">Paul M. Carvey</name>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Keshavarzian, Ali" sort="Keshavarzian, Ali" uniqKey="Keshavarzian A" first="Ali" last="Keshavarzian">Ali Keshavarzian</name>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A3">Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="4"><nlm:aff id="A4">Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, the Netherlands</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht</wicri:regionArea>
<placeName><settlement type="city">Utrecht</settlement>
<region nuts="2" type="province">Utrecht (province)</region>
</placeName>
<orgName type="university">Université d'Utrecht</orgName>
</affiliation>
</author>
<author><name sortKey="Shannon, Kathleen M" sort="Shannon, Kathleen M" uniqKey="Shannon K" first="Kathleen M." last="Shannon">Kathleen M. Shannon</name>
<affiliation wicri:level="2"><nlm:aff id="A5">Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Shaikh, Maliha" sort="Shaikh, Maliha" uniqKey="Shaikh M" first="Maliha" last="Shaikh">Maliha Shaikh</name>
<affiliation wicri:level="2"><nlm:aff id="A3">Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Internal Medicine, Division of Digestive Diseases and Nutrition, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurosurgery, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurosurgery, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pharmacology, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Kordower, Jeffrey H" sort="Kordower, Jeffrey H" uniqKey="Kordower J" first="Jeffrey H." last="Kordower">Jeffrey H. Kordower</name>
<affiliation wicri:level="2"><nlm:aff id="A5">Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurological Sciences, The Graduate College, Rush University, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><date when="2013">2013</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Brain (metabolism)</term>
<term>Brain (pathology)</term>
<term>Chromatography, Gas</term>
<term>Colon (drug effects)</term>
<term>Colon (metabolism)</term>
<term>Colon (pathology)</term>
<term>Disease Models, Animal</term>
<term>Disease Progression</term>
<term>Gastrointestinal Agents (urine)</term>
<term>Linear Models</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Parkinson Disease (etiology)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (urine)</term>
<term>Permeability (drug effects)</term>
<term>Polysaccharides (toxicity)</term>
<term>Severity of Illness Index</term>
<term>Time Factors</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>Vagus Nerve (metabolism)</term>
<term>Vagus Nerve (pathology)</term>
<term>alpha-Synuclein (metabolism)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term>
<term>alpha-Synuclein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Polysaccharides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="urine" xml:lang="en"><term>Gastrointestinal Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Colon</term>
<term>Permeability</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term>
<term>Colon</term>
<term>Parkinson Disease</term>
<term>Vagus Nerve</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term>
<term>Colon</term>
<term>Parkinson Disease</term>
<term>Vagus Nerve</term>
</keywords>
<keywords scheme="MESH" qualifier="urine" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Chromatography, Gas</term>
<term>Disease Models, Animal</term>
<term>Disease Progression</term>
<term>Linear Models</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Severity of Illness Index</term>
<term>Time Factors</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P1">Parkinson’s disease (PD) is a multifocal degenerative disorder for which there is no cure. The majority of cases are sporadic with unknown etiology. Recent data indicate that untreated patients with de novo PD have increased colonic permeability and that both de novo and premotor patients have pathological expression of α-synuclein (α-syn) in their colon. Both endpoints potentially can serve as disease biomarkers and even may initiate PD events through gut-derived, lipopolysaccharide (LPS)-induced neuronal injury. Animal models could be ideal for interrogating the potential role of the intestines in the pathogenesis of PD; however, few current animal models of PD encompass these nonmotor features. We sought to establish a progressive model of PD that includes the gastrointestinal (GI) dysfunction present in human patients. C57/BL6 mice were systemically administered one dose of either LPS (2.5 mg/kg) or saline and were sacrificed in monthly intervals (n=5 mice for 5 months) to create a time-course. Small and large intestinal permeability was assessed by analyzing the urinary output of orally ingested sugar probes through capillary column gas chromatography. α-Syn expression was assessed by counting the number of mildly, moderately, and severely affected myenteric ganglia neurons throughout the GI tract, and the counts were validated by quantitative optical density measurements. Nigrostriatal integrity was assessed by tyrosine hydroxylase immunohistochemistry stereology and densitometry. LPS caused an immediate and progressive increase in α-syn expression in the large intestine but not in the small intestine. Intestinal permeability of the whole gut (large and small intestines) progressively increased between months 2 and 4 after LPS administration but returned to baseline levels at month 5. Selective measurements demonstrated that intestinal permeability in the small intestine remained largely intact, suggesting that gut leakiness was predominately in the large intestine. Phosphorylated serine 129-α-syn was identified in a subset of colonic myenteric neurons at months 4 and 5. Although these changes were observed in the absence of nigrostriatal degeneration, an abrupt but insignificant increase in brainstem α-syn was observed that paralleled the restoration of permeability. No changes were observed over time in controls. LPS, an endotoxin used to model PD, causes sequential increases in α-syn immunoreactivity, intestinal permeability, and pathological α-syn accumulation in the colon in a manner similar to that observed in patients with PD. These features are observed without nigrostriatal degeneration and incorporate PD features before the motor syndrome. This allows for the potential use of this model in testing neuroprotective and disease-modifying therapies, including intestinal-directed therapies to fortify intestinal barrier integrity.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>Pays-Bas</li>
<li>États-Unis</li>
</country>
<region><li>Illinois</li>
<li>Utrecht (province)</li>
</region>
<settlement><li>Utrecht</li>
</settlement>
<orgName><li>Université d'Utrecht</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Illinois"><name sortKey="Kelly, Leo P" sort="Kelly, Leo P" uniqKey="Kelly L" first="Leo P." last="Kelly">Leo P. Kelly</name>
</region>
<name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name>
<name sortKey="Bakay, Roy A E" sort="Bakay, Roy A E" uniqKey="Bakay R" first="Roy A. E." last="Bakay">Roy A. E. Bakay</name>
<name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M." last="Carvey">Paul M. Carvey</name>
<name sortKey="Kelly, Leo P" sort="Kelly, Leo P" uniqKey="Kelly L" first="Leo P." last="Kelly">Leo P. Kelly</name>
<name sortKey="Keshavarzian, Ali" sort="Keshavarzian, Ali" uniqKey="Keshavarzian A" first="Ali" last="Keshavarzian">Ali Keshavarzian</name>
<name sortKey="Keshavarzian, Ali" sort="Keshavarzian, Ali" uniqKey="Keshavarzian A" first="Ali" last="Keshavarzian">Ali Keshavarzian</name>
<name sortKey="Kordower, Jeffrey H" sort="Kordower, Jeffrey H" uniqKey="Kordower J" first="Jeffrey H." last="Kordower">Jeffrey H. Kordower</name>
<name sortKey="Shaikh, Maliha" sort="Shaikh, Maliha" uniqKey="Shaikh M" first="Maliha" last="Shaikh">Maliha Shaikh</name>
<name sortKey="Shannon, Kathleen M" sort="Shannon, Kathleen M" uniqKey="Shannon K" first="Kathleen M." last="Shannon">Kathleen M. Shannon</name>
</country>
<country name="Pays-Bas"><region name="Utrecht (province)"><name sortKey="Keshavarzian, Ali" sort="Keshavarzian, Ali" uniqKey="Keshavarzian A" first="Ali" last="Keshavarzian">Ali Keshavarzian</name>
</region>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000826 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000826 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Santé |area= MovDisordV3 |flux= Main |étape= Exploration |type= RBID |clé= PMC:4050039 |texte= Progression of Intestinal Permeability Changes and Alpha-Synuclein Expression in a Mouse Model of Parkinson’s Disease }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:24898698" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a MovDisordV3
This area was generated with Dilib version V0.6.23. |