Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease
Identifieur interne : 000E68 ( Istex/Corpus ); précédent : 000E67; suivant : 000E69Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease
Auteurs : Richard B. Banati ; Susan E. Daniel ; BluntSource :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
English descriptors
Abstract
The cause and mechanism of neuronal cell death in the substantia nigra of patients with Parkinson's disease (PD) are unknown. There is also controversy about whether the cell death results from a single event followed by cell loss consistent with aging or whether there is an ongoing pathologic process. Using postmortem tissue obtained from the Parkinson's Disease Society Brain Tissue Bank in London, we have sought to establish whether apoptosis, or more specifically DNA fragmentation of neurons, is a prominent feature of nigral pathology. In addition, we have studied microglial activation in the substantia nigra as an indicator of ongoing pathology using the highly sensitive markers CR3/43 and EBM11. Reactive astrocytes have been assessed using immunostaining for glial fibrillary acidic protein (GFAP). Ten patients with pathologically proven PD were studied. In all cases, regardless of disease duration, severity, drug treatment, or age of the patient, there was no evidence of apoptosis in the substantia nigra as assessed by in situ end‐labeling of DNA fragments using biotinylated dUTP and terminal deoxynucleotidyl transferase (TdT). In contrast, a case of multiple system atrophy (MSA) served as a positive control for the technique. In this case, positive DNA end‐labeling could be found in neurons and non‐neuronal cells in the brain stem. In the PD cases, there was, however, localized pathology in the substantia nigra as revealed by the CR3/43 and EBM11 markers for activated microglia. This process seemed independent of disease duration and was florid even in patients with severe neuronal loss. It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. Future studies should focus on recent‐onset PD or incidental Lewy body disease to further address these questions.
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DOI: 10.1002/mds.870130205
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ISTEX:9A13EA9D2F2AE28EDFE0819EA5706E960F9A6FD5Le document en format XML
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Daniel</name><affiliation><mods:affiliation>Department of Neuropathology, The National Hospital for Neurology, Queen Square, London</mods:affiliation></affiliation><affiliation><mods:affiliation>The Parkinson's Disease Society Brain Tissue Bank, Institute of Neurology, London, U.K.</mods:affiliation></affiliation></author><author><name sortKey="Blunt" sort="Blunt" uniqKey="Blunt" last="Blunt">Blunt</name><affiliation><mods:affiliation>Neurosciences Division, Hammersmith Hospital Campus, Imperial College School of Medicine, London</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9A13EA9D2F2AE28EDFE0819EA5706E960F9A6FD5</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/mds.870130205</idno><idno type="url">https://api.istex.fr/document/9A13EA9D2F2AE28EDFE0819EA5706E960F9A6FD5/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000E68</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease</title><author><name sortKey="Banati, Richard B" sort="Banati, Richard B" uniqKey="Banati R" first="Richard B." last="Banati">Richard B. 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There is also controversy about whether the cell death results from a single event followed by cell loss consistent with aging or whether there is an ongoing pathologic process. Using postmortem tissue obtained from the Parkinson's Disease Society Brain Tissue Bank in London, we have sought to establish whether apoptosis, or more specifically DNA fragmentation of neurons, is a prominent feature of nigral pathology. In addition, we have studied microglial activation in the substantia nigra as an indicator of ongoing pathology using the highly sensitive markers CR3/43 and EBM11. Reactive astrocytes have been assessed using immunostaining for glial fibrillary acidic protein (GFAP). Ten patients with pathologically proven PD were studied. In all cases, regardless of disease duration, severity, drug treatment, or age of the patient, there was no evidence of apoptosis in the substantia nigra as assessed by in situ end‐labeling of DNA fragments using biotinylated dUTP and terminal deoxynucleotidyl transferase (TdT). In contrast, a case of multiple system atrophy (MSA) served as a positive control for the technique. In this case, positive DNA end‐labeling could be found in neurons and non‐neuronal cells in the brain stem. In the PD cases, there was, however, localized pathology in the substantia nigra as revealed by the CR3/43 and EBM11 markers for activated microglia. This process seemed independent of disease duration and was florid even in patients with severe neuronal loss. It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. Future studies should focus on recent‐onset PD or incidental Lewy body disease to further address these questions.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Richard B. Banati MD</name><affiliations><json:string>Neurosciences Division, Hammersmith Hospital Campus, Imperial College School of Medicine, London</json:string><json:string>Department of Neuropathology, The National Hospital for Neurology, Queen Square, London</json:string></affiliations></json:item><json:item><name>Susan E. 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It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. 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In all cases, regardless of disease duration, severity, drug treatment, or age of the patient, there was no evidence of apoptosis in the substantia nigra as assessed by in situ end‐labeling of DNA fragments using biotinylated dUTP and terminal deoxynucleotidyl transferase (TdT). In contrast, a case of multiple system atrophy (MSA) served as a positive control for the technique. In this case, positive DNA end‐labeling could be found in neurons and non‐neuronal cells in the brain stem. In the PD cases, there was, however, localized pathology in the substantia nigra as revealed by the CR3/43 and EBM11 markers for activated microglia. This process seemed independent of disease duration and was florid even in patients with severe neuronal loss. It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. Future studies should focus on recent‐onset PD or incidental Lewy body disease to further address these questions.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Microglia</term></item><item><term>Apoptosis</term></item><item><term>DNA fragmentation</term></item><item><term>Cell death mechanisms</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-03-15">Received</change><change when="1996-09-09">Registration</change><change when="1998-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9A13EA9D2F2AE28EDFE0819EA5706E960F9A6FD5/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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There is also controversy about whether the cell death results from a single event followed by cell loss consistent with aging or whether there is an ongoing pathologic process. Using postmortem tissue obtained from the Parkinson's Disease Society Brain Tissue Bank in London, we have sought to establish whether apoptosis, or more specifically DNA fragmentation of neurons, is a prominent feature of nigral pathology. In addition, we have studied microglial activation in the substantia nigra as an indicator of ongoing pathology using the highly sensitive markers CR3/43 and EBM11. Reactive astrocytes have been assessed using immunostaining for glial fibrillary acidic protein (GFAP). Ten patients with pathologically proven PD were studied. In all cases, regardless of disease duration, severity, drug treatment, or age of the patient, there was no evidence of apoptosis in the substantia nigra as assessed by in situ end‐labeling of DNA fragments using biotinylated dUTP and terminal deoxynucleotidyl transferase (TdT). In contrast, a case of multiple system atrophy (MSA) served as a positive control for the technique. In this case, positive DNA end‐labeling could be found in neurons and non‐neuronal cells in the brain stem. In the PD cases, there was, however, localized pathology in the substantia nigra as revealed by the CR3/43 and EBM11 markers for activated microglia. This process seemed independent of disease duration and was florid even in patients with severe neuronal loss. It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. Future studies should focus on recent‐onset PD or incidental Lewy body disease to further address these questions.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GLIAL PATHOLOGY BUT ABSENCE OF APOPTOTIC NIGRAL NEURONS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Richard B.</namePart><namePart type="family">Banati</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurosciences Division, Hammersmith Hospital Campus, Imperial College School of Medicine, London</affiliation><affiliation>Department of Neuropathology, The National Hospital for Neurology, Queen Square, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan E.</namePart><namePart type="family">Daniel</namePart><namePart type="termsOfAddress">MRCPath</namePart><affiliation>Department of Neuropathology, The National Hospital for Neurology, Queen Square, London</affiliation><affiliation>The Parkinson's Disease Society Brain Tissue Bank, Institute of Neurology, London, U.K.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Blunt</namePart><namePart type="termsOfAddress">MRCP</namePart><affiliation>Neurosciences Division, Hammersmith Hospital Campus, Imperial College School of Medicine, London</affiliation><description>Correspondence: The Neurosciences Division, Hammersmith Hospital, Imperial College School of Medicine, London W12 OHS, UK</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-03</dateIssued><dateCaptured encoding="w3cdtf">1996-03-15</dateCaptured><dateValid encoding="w3cdtf">1996-09-09</dateValid><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">2</extent><extent unit="references">21</extent></physicalDescription><abstract lang="en">The cause and mechanism of neuronal cell death in the substantia nigra of patients with Parkinson's disease (PD) are unknown. There is also controversy about whether the cell death results from a single event followed by cell loss consistent with aging or whether there is an ongoing pathologic process. Using postmortem tissue obtained from the Parkinson's Disease Society Brain Tissue Bank in London, we have sought to establish whether apoptosis, or more specifically DNA fragmentation of neurons, is a prominent feature of nigral pathology. In addition, we have studied microglial activation in the substantia nigra as an indicator of ongoing pathology using the highly sensitive markers CR3/43 and EBM11. Reactive astrocytes have been assessed using immunostaining for glial fibrillary acidic protein (GFAP). Ten patients with pathologically proven PD were studied. In all cases, regardless of disease duration, severity, drug treatment, or age of the patient, there was no evidence of apoptosis in the substantia nigra as assessed by in situ end‐labeling of DNA fragments using biotinylated dUTP and terminal deoxynucleotidyl transferase (TdT). In contrast, a case of multiple system atrophy (MSA) served as a positive control for the technique. In this case, positive DNA end‐labeling could be found in neurons and non‐neuronal cells in the brain stem. In the PD cases, there was, however, localized pathology in the substantia nigra as revealed by the CR3/43 and EBM11 markers for activated microglia. This process seemed independent of disease duration and was florid even in patients with severe neuronal loss. It remains to be determined to what extent the activation of glial cells reflects progressive nigral pathology, and whether those factors which are classically associated with prominent apoptotic neuronal cell death in vivo, such as neurotrophic factor deprivation, are prime causes of nigral neuronal loss in PD. Future studies should focus on recent‐onset PD or incidental Lewy body disease to further address these questions.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Microglia</topic><topic>Apoptosis</topic><topic>DNA fragmentation</topic><topic>Cell death mechanisms</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>221</start><end>227</end><total>7</total></extent></part></relatedItem><identifier type="istex">9A13EA9D2F2AE28EDFE0819EA5706E960F9A6FD5</identifier><identifier type="DOI">10.1002/mds.870130205</identifier><identifier type="ArticleID">MDS870130205</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Glial pathology but absence of apoptotic nigral neurons in long‐standing Parkinson's disease
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