Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.
Identifieur interne : 000406 ( PubMed/Corpus ); précédent : 000405; suivant : 000407Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.
Auteurs : Junchao Tong ; Lee-Cyn Ang ; Belinda Williams ; Yoshiaki Furukawa ; Paul Fitzmaurice ; Mark Guttman ; Isabelle Boileau ; Oleh Hornykiewicz ; Stephen J. KishSource :
- Neurobiology of disease [ 1095-953X ] ; 2015.
English descriptors
- KwdEn :
- Aged, Astrocytes (metabolism), Biomarkers (metabolism), Blotting, Western, Caudate Nucleus (metabolism), Electrophoresis, Polyacrylamide Gel, Frontal Lobe (metabolism), Glial Fibrillary Acidic Protein (metabolism), HSP27 Heat-Shock Proteins (metabolism), Humans, Multiple System Atrophy (metabolism), Parkinson Disease (metabolism), Putamen (metabolism), Supranuclear Palsy, Progressive (metabolism), Vimentin (metabolism).
- MESH :
- chemical , metabolism : Biomarkers, Glial Fibrillary Acidic Protein, HSP27 Heat-Shock Proteins, Vimentin.
- metabolism : Astrocytes, Caudate Nucleus, Frontal Lobe, Multiple System Atrophy, Parkinson Disease, Putamen, Supranuclear Palsy, Progressive.
- Aged, Blotting, Western, Electrophoresis, Polyacrylamide Gel, Humans.
Abstract
Although gliosis is a normal response to brain injury, reports on the extent of astrogliosis in the degenerating substantia nigra in Parkinson's disease (PD) are conflicting. It has also been recently suggested that accumulation of nigral α-synuclein in this disorder might suppress astrocyte activation which in turn could exacerbate the degenerative process. This study examined brain protein levels (intact protein, fragments, and aggregates, if any) of astroglial markers and their relationship to α-synuclein in PD and in the positive control parkinson-plus conditions multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Autopsied brain homogenates of patients with PD (n=10), MSA (n=11), PSP (n=11) and matched controls (n=10) were examined for the astroglial markers glial fibrillary acidic protein (GFAP), vimentin, and heat shock protein-27 (Hsp27) by quantitative immunoblotting. As expected, both MSA (putamen>substantia nigra>caudate>frontal cortex) and PSP (substantia nigra>caudate>putamen, frontal cortex) showed widespread but regionally specific pattern of increased immunoreactivity of the markers, in particular for the partially proteolyzed fragments (all three) and aggregates (GFAP). In contrast, immunoreactivity of the three markers was largely normal in PD in brain regions examined with the exception of trends for variably increased levels of cleaved vimentin in substantia nigra and frontal cortex. In patients with PD, GFAP levels in the substantia nigra correlated inversely with α-synuclein accumulation whereas the opposite was true for MSA. Our biochemical findings of generally normal protein levels of astroglial markers in substantia nigra of PD, and negative correlation with α-synuclein concentration, are consistent with some recent neuropathology reports of mild astroglial response and with the speculation that astrogliosis might be suppressed in this disorder by excessive α-synuclein accumulation. Should astrogliosis protect, to some extent, the degenerating substantia nigra from damage, therapeutics aimed at normalization of astrocyte reaction in PD could be helpful.
DOI: 10.1016/j.nbd.2015.06.010
PubMed: 26102022
Links to Exploration step
pubmed:26102022Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.</title><author><name sortKey="Tong, Junchao" sort="Tong, Junchao" uniqKey="Tong J" first="Junchao" last="Tong">Junchao Tong</name><affiliation><nlm:affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Electronic address: junchao.tong@camh.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Ang, Lee Cyn" sort="Ang, Lee Cyn" uniqKey="Ang L" first="Lee-Cyn" last="Ang">Lee-Cyn Ang</name><affiliation><nlm:affiliation>Division of Neuropathology, London Health Science Centre, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Williams, Belinda" sort="Williams, Belinda" uniqKey="Williams B" first="Belinda" last="Williams">Belinda Williams</name><affiliation><nlm:affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name><affiliation><nlm:affiliation>Department of Neurology, Juntendo Tokyo Koto Geriatric Medical Center, and Faculty of Medicine, University & Post Graduate University of Juntendo, Tokyo, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Fitzmaurice, Paul" sort="Fitzmaurice, Paul" uniqKey="Fitzmaurice P" first="Paul" last="Fitzmaurice">Paul Fitzmaurice</name><affiliation><nlm:affiliation>The Drug Detection Agency, Auckland, New Zealand.</nlm:affiliation></affiliation></author><author><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name><affiliation><nlm:affiliation>Centre for Movement Disorders, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Boileau, Isabelle" sort="Boileau, Isabelle" uniqKey="Boileau I" first="Isabelle" last="Boileau">Isabelle Boileau</name><affiliation><nlm:affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><affiliation><nlm:affiliation>Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria.</nlm:affiliation></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J" last="Kish">Stephen J. Kish</name><affiliation><nlm:affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26102022</idno><idno type="pmid">26102022</idno><idno type="doi">10.1016/j.nbd.2015.06.010</idno><idno type="wicri:Area/PubMed/Corpus">000406</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000406</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.</title><author><name sortKey="Tong, Junchao" sort="Tong, Junchao" uniqKey="Tong J" first="Junchao" last="Tong">Junchao Tong</name><affiliation><nlm:affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Electronic address: junchao.tong@camh.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Ang, Lee Cyn" sort="Ang, Lee Cyn" uniqKey="Ang L" first="Lee-Cyn" last="Ang">Lee-Cyn Ang</name><affiliation><nlm:affiliation>Division of Neuropathology, London Health Science Centre, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Williams, Belinda" sort="Williams, Belinda" uniqKey="Williams B" first="Belinda" last="Williams">Belinda Williams</name><affiliation><nlm:affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name><affiliation><nlm:affiliation>Department of Neurology, Juntendo Tokyo Koto Geriatric Medical Center, and Faculty of Medicine, University & Post Graduate University of Juntendo, Tokyo, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Fitzmaurice, Paul" sort="Fitzmaurice, Paul" uniqKey="Fitzmaurice P" first="Paul" last="Fitzmaurice">Paul Fitzmaurice</name><affiliation><nlm:affiliation>The Drug Detection Agency, Auckland, New Zealand.</nlm:affiliation></affiliation></author><author><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name><affiliation><nlm:affiliation>Centre for Movement Disorders, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Boileau, Isabelle" sort="Boileau, Isabelle" uniqKey="Boileau I" first="Isabelle" last="Boileau">Isabelle Boileau</name><affiliation><nlm:affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><affiliation><nlm:affiliation>Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria.</nlm:affiliation></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J" last="Kish">Stephen J. Kish</name><affiliation><nlm:affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Astrocytes (metabolism)</term><term>Biomarkers (metabolism)</term><term>Blotting, Western</term><term>Caudate Nucleus (metabolism)</term><term>Electrophoresis, Polyacrylamide Gel</term><term>Frontal Lobe (metabolism)</term><term>Glial Fibrillary Acidic Protein (metabolism)</term><term>HSP27 Heat-Shock Proteins (metabolism)</term><term>Humans</term><term>Multiple System Atrophy (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Putamen (metabolism)</term><term>Supranuclear Palsy, Progressive (metabolism)</term><term>Vimentin (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>Glial Fibrillary Acidic Protein</term><term>HSP27 Heat-Shock Proteins</term><term>Vimentin</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Caudate Nucleus</term><term>Frontal Lobe</term><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Putamen</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Blotting, Western</term><term>Electrophoresis, Polyacrylamide Gel</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although gliosis is a normal response to brain injury, reports on the extent of astrogliosis in the degenerating substantia nigra in Parkinson's disease (PD) are conflicting. It has also been recently suggested that accumulation of nigral α-synuclein in this disorder might suppress astrocyte activation which in turn could exacerbate the degenerative process. This study examined brain protein levels (intact protein, fragments, and aggregates, if any) of astroglial markers and their relationship to α-synuclein in PD and in the positive control parkinson-plus conditions multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Autopsied brain homogenates of patients with PD (n=10), MSA (n=11), PSP (n=11) and matched controls (n=10) were examined for the astroglial markers glial fibrillary acidic protein (GFAP), vimentin, and heat shock protein-27 (Hsp27) by quantitative immunoblotting. As expected, both MSA (putamen>substantia nigra>caudate>frontal cortex) and PSP (substantia nigra>caudate>putamen, frontal cortex) showed widespread but regionally specific pattern of increased immunoreactivity of the markers, in particular for the partially proteolyzed fragments (all three) and aggregates (GFAP). In contrast, immunoreactivity of the three markers was largely normal in PD in brain regions examined with the exception of trends for variably increased levels of cleaved vimentin in substantia nigra and frontal cortex. In patients with PD, GFAP levels in the substantia nigra correlated inversely with α-synuclein accumulation whereas the opposite was true for MSA. Our biochemical findings of generally normal protein levels of astroglial markers in substantia nigra of PD, and negative correlation with α-synuclein concentration, are consistent with some recent neuropathology reports of mild astroglial response and with the speculation that astrogliosis might be suppressed in this disorder by excessive α-synuclein accumulation. Should astrogliosis protect, to some extent, the degenerating substantia nigra from damage, therapeutics aimed at normalization of astrocyte reaction in PD could be helpful.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26102022</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>09</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>82</Volume><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.</ArticleTitle><Pagination><MedlinePgn>243-53</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2015.06.010</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(15)00228-4</ELocationID><Abstract><AbstractText>Although gliosis is a normal response to brain injury, reports on the extent of astrogliosis in the degenerating substantia nigra in Parkinson's disease (PD) are conflicting. It has also been recently suggested that accumulation of nigral α-synuclein in this disorder might suppress astrocyte activation which in turn could exacerbate the degenerative process. This study examined brain protein levels (intact protein, fragments, and aggregates, if any) of astroglial markers and their relationship to α-synuclein in PD and in the positive control parkinson-plus conditions multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Autopsied brain homogenates of patients with PD (n=10), MSA (n=11), PSP (n=11) and matched controls (n=10) were examined for the astroglial markers glial fibrillary acidic protein (GFAP), vimentin, and heat shock protein-27 (Hsp27) by quantitative immunoblotting. As expected, both MSA (putamen>substantia nigra>caudate>frontal cortex) and PSP (substantia nigra>caudate>putamen, frontal cortex) showed widespread but regionally specific pattern of increased immunoreactivity of the markers, in particular for the partially proteolyzed fragments (all three) and aggregates (GFAP). In contrast, immunoreactivity of the three markers was largely normal in PD in brain regions examined with the exception of trends for variably increased levels of cleaved vimentin in substantia nigra and frontal cortex. In patients with PD, GFAP levels in the substantia nigra correlated inversely with α-synuclein accumulation whereas the opposite was true for MSA. Our biochemical findings of generally normal protein levels of astroglial markers in substantia nigra of PD, and negative correlation with α-synuclein concentration, are consistent with some recent neuropathology reports of mild astroglial response and with the speculation that astrogliosis might be suppressed in this disorder by excessive α-synuclein accumulation. Should astrogliosis protect, to some extent, the degenerating substantia nigra from damage, therapeutics aimed at normalization of astrocyte reaction in PD could be helpful.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Junchao</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Electronic address: junchao.tong@camh.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ang</LastName><ForeName>Lee-Cyn</ForeName><Initials>LC</Initials><AffiliationInfo><Affiliation>Division of Neuropathology, London Health Science Centre, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Belinda</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Furukawa</LastName><ForeName>Yoshiaki</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurology, Juntendo Tokyo Koto Geriatric Medical Center, and Faculty of Medicine, University & Post Graduate University of Juntendo, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fitzmaurice</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The Drug Detection Agency, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guttman</LastName><ForeName>Mark</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Centre for Movement Disorders, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boileau</LastName><ForeName>Isabelle</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Addiction Imaging Research Group, Campbell Family Mental Health Research Institute, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hornykiewicz</LastName><ForeName>Oleh</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kish</LastName><ForeName>Stephen J</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 DA025096</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DA07182</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005904">Glial Fibrillary Acidic Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D055551">HSP27 Heat-Shock Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C057725">HSPB1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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