Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.
Identifieur interne : 001484 ( PubMed/Checkpoint ); précédent : 001483; suivant : 001485Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.
Auteurs : V. Buée-Scherrer [France] ; L. Buée ; P R Hof ; B. Leveugle ; C. Gilles ; A J Loerzel ; D P Perl ; A. DelacourteSource :
- The American journal of pathology [ 0002-9440 ] ; 1995.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Amyotrophic Lateral Sclerosis (metabolism), Amyotrophic Lateral Sclerosis (pathology), Dementia (metabolism), Dementia (pathology), Guam, Humans, Immune Sera, Immunoblotting, Middle Aged, Neurofibrillary Tangles (chemistry), Parkinson Disease (metabolism), Parkinson Disease (pathology), tau Proteins (analysis).
- MESH :
- chemical , analysis : tau Proteins.
- chemical : Immune Sera.
- geographic : Guam.
- chemistry : Neurofibrillary Tangles.
- metabolism : Amyotrophic Lateral Sclerosis, Dementia, Parkinson Disease.
- pathology : Amyotrophic Lateral Sclerosis, Dementia, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Humans, Immunoblotting, Middle Aged.
Abstract
Neurofibrillary tangles are observed in several neurodegenerative disorders including Alzheimer's disease, progressive supranuclear palsy, and amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. The major components of neurofibrillary tangles are hyperphosphorylated tau proteins that can be directly detected in brain homogenates, using immunoblotting with specific immunological probes. To investigate whether tau proteins differ biochemically among various neurodegenerative disorders, we analyzed a series of brain samples from Guamanian patients in comparison with Alzheimer's disease, progressive supranuclear palsy, and normal aging. In Alzheimer's disease, these hyperphosphorylated tau proteins are composed of a triplet referred to as tau 55, 64, and 69, whereas in progressive supranuclear palsy, neurofibrillary degeneration is characterized by a tau doublet (tau 64 and 69). In the present study, characterization of tau proteins was performed by immunoblotting, on different cortical and subcortical regions of postmortem brain specimens from Guamanian natives. In all of the cases, biochemical data were always consistent with neuropathological findings. In contrast to Alzheimer's disease patients where the tau triplet is found mostly in cortical regions, a similar triplet was strongly detected in both cortical and subcortical areas in Guamanian patients. The tau profile differed quantitatively from case to case demonstrating that the Alzheimer's disease-related tau triplet had a heterogeneous regional distribution. These data suggest that the tau triplet found in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam is similar to that observed in Alzheimer's disease, and the regional distribution of tau proteins differs in these disorders.
PubMed: 7717459
Affiliations:
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Delacourte</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1995">1995</date><idno type="RBID">pubmed:7717459</idno><idno type="pmid">7717459</idno><idno type="wicri:Area/PubMed/Corpus">001635</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001635</idno><idno type="wicri:Area/PubMed/Curation">001594</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001594</idno><idno type="wicri:Area/PubMed/Checkpoint">001594</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001594</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.</title><author><name sortKey="Buee Scherrer, V" sort="Buee Scherrer, V" uniqKey="Buee Scherrer V" first="V" last="Buée-Scherrer">V. Buée-Scherrer</name><affiliation wicri:level="3"><nlm:affiliation>INSERM U422, Lille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U422, Lille</wicri:regionArea><placeName><region type="region">Hauts-de-France</region><region type="old region">Nord-Pas-de-Calais</region><settlement type="city">Lille</settlement></placeName></affiliation></author><author><name sortKey="Buee, L" sort="Buee, L" uniqKey="Buee L" first="L" last="Buée">L. Buée</name></author><author><name sortKey="Hof, P R" sort="Hof, P R" uniqKey="Hof P" first="P R" last="Hof">P R Hof</name></author><author><name sortKey="Leveugle, B" sort="Leveugle, B" uniqKey="Leveugle B" first="B" last="Leveugle">B. Leveugle</name></author><author><name sortKey="Gilles, C" sort="Gilles, C" uniqKey="Gilles C" first="C" last="Gilles">C. Gilles</name></author><author><name sortKey="Loerzel, A J" sort="Loerzel, A J" uniqKey="Loerzel A" first="A J" last="Loerzel">A J Loerzel</name></author><author><name sortKey="Perl, D P" sort="Perl, D P" uniqKey="Perl D" first="D P" last="Perl">D P Perl</name></author><author><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name></author></analytic><series><title level="j">The American journal of pathology</title><idno type="ISSN">0002-9440</idno><imprint><date when="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Amyotrophic Lateral Sclerosis (metabolism)</term><term>Amyotrophic Lateral Sclerosis (pathology)</term><term>Dementia (metabolism)</term><term>Dementia (pathology)</term><term>Guam</term><term>Humans</term><term>Immune Sera</term><term>Immunoblotting</term><term>Middle Aged</term><term>Neurofibrillary Tangles (chemistry)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>tau Proteins (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Immune Sera</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Guam</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Neurofibrillary Tangles</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Humans</term><term>Immunoblotting</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurofibrillary tangles are observed in several neurodegenerative disorders including Alzheimer's disease, progressive supranuclear palsy, and amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. The major components of neurofibrillary tangles are hyperphosphorylated tau proteins that can be directly detected in brain homogenates, using immunoblotting with specific immunological probes. To investigate whether tau proteins differ biochemically among various neurodegenerative disorders, we analyzed a series of brain samples from Guamanian patients in comparison with Alzheimer's disease, progressive supranuclear palsy, and normal aging. In Alzheimer's disease, these hyperphosphorylated tau proteins are composed of a triplet referred to as tau 55, 64, and 69, whereas in progressive supranuclear palsy, neurofibrillary degeneration is characterized by a tau doublet (tau 64 and 69). In the present study, characterization of tau proteins was performed by immunoblotting, on different cortical and subcortical regions of postmortem brain specimens from Guamanian natives. In all of the cases, biochemical data were always consistent with neuropathological findings. In contrast to Alzheimer's disease patients where the tau triplet is found mostly in cortical regions, a similar triplet was strongly detected in both cortical and subcortical areas in Guamanian patients. The tau profile differed quantitatively from case to case demonstrating that the Alzheimer's disease-related tau triplet had a heterogeneous regional distribution. These data suggest that the tau triplet found in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam is similar to that observed in Alzheimer's disease, and the regional distribution of tau proteins differs in these disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7717459</PMID><DateCreated><Year>1995</Year><Month>05</Month><Day>12</Day></DateCreated><DateCompleted><Year>1995</Year><Month>05</Month><Day>12</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0002-9440</ISSN><JournalIssue CitedMedium="Print"><Volume>146</Volume><Issue>4</Issue><PubDate><Year>1995</Year><Month>Apr</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.</ArticleTitle><Pagination><MedlinePgn>924-32</MedlinePgn></Pagination><Abstract><AbstractText>Neurofibrillary tangles are observed in several neurodegenerative disorders including Alzheimer's disease, progressive supranuclear palsy, and amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. The major components of neurofibrillary tangles are hyperphosphorylated tau proteins that can be directly detected in brain homogenates, using immunoblotting with specific immunological probes. To investigate whether tau proteins differ biochemically among various neurodegenerative disorders, we analyzed a series of brain samples from Guamanian patients in comparison with Alzheimer's disease, progressive supranuclear palsy, and normal aging. In Alzheimer's disease, these hyperphosphorylated tau proteins are composed of a triplet referred to as tau 55, 64, and 69, whereas in progressive supranuclear palsy, neurofibrillary degeneration is characterized by a tau doublet (tau 64 and 69). In the present study, characterization of tau proteins was performed by immunoblotting, on different cortical and subcortical regions of postmortem brain specimens from Guamanian natives. In all of the cases, biochemical data were always consistent with neuropathological findings. In contrast to Alzheimer's disease patients where the tau triplet is found mostly in cortical regions, a similar triplet was strongly detected in both cortical and subcortical areas in Guamanian patients. The tau profile differed quantitatively from case to case demonstrating that the Alzheimer's disease-related tau triplet had a heterogeneous regional distribution. These data suggest that the tau triplet found in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam is similar to that observed in Alzheimer's disease, and the regional distribution of tau proteins differs in these disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Buée-Scherrer</LastName><ForeName>V</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>INSERM U422, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buée</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Hof</LastName><ForeName>P R</ForeName><Initials>PR</Initials></Author><Author ValidYN="Y"><LastName>Leveugle</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gilles</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Loerzel</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Perl</LastName><ForeName>D P</ForeName><Initials>DP</Initials></Author><Author ValidYN="Y"><LastName>Delacourte</LastName><ForeName>A</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AG05138</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG08802</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007106">Immune Sera</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Acta Neuropathol. 1994;88(5):397-404</RefSource><PMID Version="1">7847067</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 1994 Dec;145(6):1496-508</RefSource><PMID Version="1">7992852</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1966 Apr;14(4):356-68</RefSource><PMID Version="1">5906460</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1966 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MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003704" MajorTopicYN="N">Dementia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006141" MajorTopicYN="N" Type="Geographic">Guam</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007106" MajorTopicYN="N">Immune Sera</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015151" MajorTopicYN="N">Immunoblotting</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016874" MajorTopicYN="N">Neurofibrillary Tangles</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="Y">analysis</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC1869250</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1995</Year><Month>4</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1995</Year><Month>4</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1995</Year><Month>4</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">7717459</ArticleId><ArticleId IdType="pmc">PMC1869250</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Hauts-de-France</li><li>Nord-Pas-de-Calais</li></region><settlement><li>Lille</li></settlement></list><tree><noCountry><name sortKey="Buee, L" sort="Buee, L" uniqKey="Buee L" first="L" last="Buée">L. Buée</name><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name><name sortKey="Gilles, C" sort="Gilles, C" uniqKey="Gilles C" first="C" last="Gilles">C. Gilles</name><name sortKey="Hof, P R" sort="Hof, P R" uniqKey="Hof P" first="P R" last="Hof">P R Hof</name><name sortKey="Leveugle, B" sort="Leveugle, B" uniqKey="Leveugle B" first="B" last="Leveugle">B. Leveugle</name><name sortKey="Loerzel, A J" sort="Loerzel, A J" uniqKey="Loerzel A" first="A J" last="Loerzel">A J Loerzel</name><name sortKey="Perl, D P" sort="Perl, D P" uniqKey="Perl D" first="D P" last="Perl">D P Perl</name></noCountry><country name="France"><region name="Hauts-de-France"><name sortKey="Buee Scherrer, V" sort="Buee Scherrer, V" uniqKey="Buee Scherrer V" first="V" last="Buée-Scherrer">V. Buée-Scherrer</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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