Tau pathology in a family with dementia and a P301L mutation in tau.
Identifieur interne : 001618 ( PubMed/Checkpoint ); précédent : 001617; suivant : 001619Tau pathology in a family with dementia and a P301L mutation in tau.
Auteurs : S S Mirra [États-Unis] ; J R Murrell ; M. Gearing ; M G Spillantini ; M. Goedert ; R A Crowther ; A I Levey ; R. Jones ; J. Green ; J M Shoffner ; B H Wainer ; M L Schmidt ; J Q Trojanowski ; B. GhettiSource :
- Journal of neuropathology and experimental neurology [ 0022-3069 ] ; 1999.
Descripteurs français
English descriptors
- KwdEn :
- Atrophy, Blotting, Western, Canada, DNA Mutational Analysis, DNA Probes, Dementia (genetics), Dementia (pathology), Epitopes (genetics), Family Health, Female, France, Frontal Lobe (pathology), Humans, Male, Microscopy, Electron, Middle Aged, Neurofibrillary Tangles (chemistry), Neurofibrillary Tangles (ultrastructure), Neurons (chemistry), Neurons (pathology), Parietal Lobe (pathology), Parkinson Disease (genetics), Parkinson Disease (pathology), Pedigree, Point Mutation, Polymerase Chain Reaction, Restriction Mapping, Solubility, Temporal Lobe (pathology), tau Proteins (analysis), tau Proteins (genetics).
- MESH :
- chemical , analysis : tau Proteins.
- chemical , genetics : Epitopes, tau Proteins.
- chemical : DNA Probes.
- geographic : Canada, France.
- chemistry : Neurofibrillary Tangles, Neurons.
- genetics : Dementia, Parkinson Disease.
- pathology : Dementia, Frontal Lobe, Neurons, Parietal Lobe, Parkinson Disease, Temporal Lobe.
- ultrastructure : Neurofibrillary Tangles.
- Atrophy, Blotting, Western, DNA Mutational Analysis, Family Health, Female, Humans, Male, Microscopy, Electron, Middle Aged, Pedigree, Point Mutation, Polymerase Chain Reaction, Restriction Mapping, Solubility.
Abstract
Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene. Here we report our findings on 2 affected siblings from a family with early-onset dementia, characterized by extensive tau pathology and a Pro to Leu mutation at codon 301 of tau. The proband, a 55-year-old woman, and her 63-year-old brother died after a progressive dementing illness clinically diagnosed as Alzheimer disease. Their mother, 2 sisters, maternal aunt and uncle, and several cousins were also affected. Autopsy in both cases revealed frontotemporal atrophy and degeneration of basal ganglia and substantia nigra. Sequencing of exon 10 of the tau gene revealed a C to T transition at codon 301, resulting in a Pro to Leu substitution. Widespread neuronal and glial inclusions, neuropil threads, and astrocytic plaques similar to those seen in corticobasal degeneration were labeled with a battery of antibodies to phosphorylation-dependent and phosphorylation-independent epitopes spanning the entire tau sequence. Isolated tau filaments had the morphology of narrow twisted ribbons. Sarkosyl-insoluble tau exhibited 2 major bands of 64 and 68 kDa and a minor 72 kDa band, similar to the pattern seen in a familial tauopathy associated with an intronic tau mutation. These pathological tau bands predominantly contained the subset of tau isoforms with 4 microtubule-binding repeats selectively affected by the P301L missense mutation. Our findings emphasize the phenotypic and genetic heterogeneity of tauopathies and highlight intriguing links between FTDP-17 and other neurodegenerative diseases.
PubMed: 10218629
Affiliations:
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Gearing</name></author><author><name sortKey="Spillantini, M G" sort="Spillantini, M G" uniqKey="Spillantini M" first="M G" last="Spillantini">M G Spillantini</name></author><author><name sortKey="Goedert, M" sort="Goedert, M" uniqKey="Goedert M" first="M" last="Goedert">M. Goedert</name></author><author><name sortKey="Crowther, R A" sort="Crowther, R A" uniqKey="Crowther R" first="R A" last="Crowther">R A Crowther</name></author><author><name sortKey="Levey, A I" sort="Levey, A I" uniqKey="Levey A" first="A I" last="Levey">A I Levey</name></author><author><name sortKey="Jones, R" sort="Jones, R" uniqKey="Jones R" first="R" last="Jones">R. Jones</name></author><author><name sortKey="Green, J" sort="Green, J" uniqKey="Green J" first="J" last="Green">J. Green</name></author><author><name sortKey="Shoffner, J M" sort="Shoffner, J M" uniqKey="Shoffner J" first="J M" last="Shoffner">J M Shoffner</name></author><author><name sortKey="Wainer, B H" sort="Wainer, B H" uniqKey="Wainer B" first="B H" last="Wainer">B H Wainer</name></author><author><name sortKey="Schmidt, M L" sort="Schmidt, M L" uniqKey="Schmidt M" first="M L" last="Schmidt">M L Schmidt</name></author><author><name sortKey="Trojanowski, J Q" sort="Trojanowski, J Q" uniqKey="Trojanowski J" first="J Q" last="Trojanowski">J Q Trojanowski</name></author><author><name sortKey="Ghetti, B" sort="Ghetti, B" uniqKey="Ghetti B" first="B" last="Ghetti">B. Ghetti</name></author></analytic><series><title level="j">Journal of neuropathology and experimental neurology</title><idno type="ISSN">0022-3069</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atrophy</term><term>Blotting, Western</term><term>Canada</term><term>DNA Mutational Analysis</term><term>DNA Probes</term><term>Dementia (genetics)</term><term>Dementia (pathology)</term><term>Epitopes (genetics)</term><term>Family Health</term><term>Female</term><term>France</term><term>Frontal Lobe (pathology)</term><term>Humans</term><term>Male</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Neurofibrillary Tangles (chemistry)</term><term>Neurofibrillary Tangles (ultrastructure)</term><term>Neurons (chemistry)</term><term>Neurons (pathology)</term><term>Parietal Lobe (pathology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Pedigree</term><term>Point Mutation</term><term>Polymerase Chain Reaction</term><term>Restriction Mapping</term><term>Solubility</term><term>Temporal Lobe (pathology)</term><term>tau Proteins (analysis)</term><term>tau Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Epitopes</term><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DNA Probes</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Canada</term><term>France</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Neurofibrillary Tangles</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dementia</term><term>Frontal Lobe</term><term>Neurons</term><term>Parietal Lobe</term><term>Parkinson Disease</term><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Neurofibrillary Tangles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Atrophy</term><term>Blotting, Western</term><term>DNA Mutational Analysis</term><term>Family Health</term><term>Female</term><term>Humans</term><term>Male</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Pedigree</term><term>Point Mutation</term><term>Polymerase Chain Reaction</term><term>Restriction Mapping</term><term>Solubility</term></keywords><keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>Canada</term><term>France</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene. Here we report our findings on 2 affected siblings from a family with early-onset dementia, characterized by extensive tau pathology and a Pro to Leu mutation at codon 301 of tau. The proband, a 55-year-old woman, and her 63-year-old brother died after a progressive dementing illness clinically diagnosed as Alzheimer disease. Their mother, 2 sisters, maternal aunt and uncle, and several cousins were also affected. Autopsy in both cases revealed frontotemporal atrophy and degeneration of basal ganglia and substantia nigra. Sequencing of exon 10 of the tau gene revealed a C to T transition at codon 301, resulting in a Pro to Leu substitution. Widespread neuronal and glial inclusions, neuropil threads, and astrocytic plaques similar to those seen in corticobasal degeneration were labeled with a battery of antibodies to phosphorylation-dependent and phosphorylation-independent epitopes spanning the entire tau sequence. Isolated tau filaments had the morphology of narrow twisted ribbons. Sarkosyl-insoluble tau exhibited 2 major bands of 64 and 68 kDa and a minor 72 kDa band, similar to the pattern seen in a familial tauopathy associated with an intronic tau mutation. These pathological tau bands predominantly contained the subset of tau isoforms with 4 microtubule-binding repeats selectively affected by the P301L missense mutation. Our findings emphasize the phenotypic and genetic heterogeneity of tauopathies and highlight intriguing links between FTDP-17 and other neurodegenerative diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10218629</PMID><DateCreated><Year>1999</Year><Month>05</Month><Day>06</Day></DateCreated><DateCompleted><Year>1999</Year><Month>05</Month><Day>06</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3069</ISSN><JournalIssue CitedMedium="Print"><Volume>58</Volume><Issue>4</Issue><PubDate><Year>1999</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Journal of neuropathology and experimental neurology</Title><ISOAbbreviation>J. Neuropathol. Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Tau pathology in a family with dementia and a P301L mutation in tau.</ArticleTitle><Pagination><MedlinePgn>335-45</MedlinePgn></Pagination><Abstract><AbstractText>Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene. Here we report our findings on 2 affected siblings from a family with early-onset dementia, characterized by extensive tau pathology and a Pro to Leu mutation at codon 301 of tau. The proband, a 55-year-old woman, and her 63-year-old brother died after a progressive dementing illness clinically diagnosed as Alzheimer disease. Their mother, 2 sisters, maternal aunt and uncle, and several cousins were also affected. Autopsy in both cases revealed frontotemporal atrophy and degeneration of basal ganglia and substantia nigra. Sequencing of exon 10 of the tau gene revealed a C to T transition at codon 301, resulting in a Pro to Leu substitution. Widespread neuronal and glial inclusions, neuropil threads, and astrocytic plaques similar to those seen in corticobasal degeneration were labeled with a battery of antibodies to phosphorylation-dependent and phosphorylation-independent epitopes spanning the entire tau sequence. Isolated tau filaments had the morphology of narrow twisted ribbons. Sarkosyl-insoluble tau exhibited 2 major bands of 64 and 68 kDa and a minor 72 kDa band, similar to the pattern seen in a familial tauopathy associated with an intronic tau mutation. These pathological tau bands predominantly contained the subset of tau isoforms with 4 microtubule-binding repeats selectively affected by the P301L missense mutation. Our findings emphasize the phenotypic and genetic heterogeneity of tauopathies and highlight intriguing links between FTDP-17 and other neurodegenerative diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mirra</LastName><ForeName>S S</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Department of Pathology, State University of New York, Health Science Center at Brooklyn, 11203, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murrell</LastName><ForeName>J R</ForeName><Initials>JR</Initials></Author><Author ValidYN="Y"><LastName>Gearing</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Spillantini</LastName><ForeName>M G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Goedert</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Crowther</LastName><ForeName>R A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Levey</LastName><ForeName>A I</ForeName><Initials>AI</Initials></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Green</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Shoffner</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Wainer</LastName><ForeName>B H</ForeName><Initials>BH</Initials></Author><Author ValidYN="Y"><LastName>Schmidt</LastName><ForeName>M L</ForeName><Initials>ML</Initials></Author><Author ValidYN="Y"><LastName>Trojanowski</LastName><ForeName>J Q</ForeName><Initials>JQ</Initials></Author><Author ValidYN="Y"><LastName>Ghetti</LastName><ForeName>B</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="N"><Grant><GrantID>AG10124</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG10130</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG10133</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><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>England</Country><MedlineTA>J Neuropathol Exp Neurol</MedlineTA><NlmUniqueID>2985192R</NlmUniqueID><ISSNLinking>0022-3069</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015342">DNA Probes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001284" MajorTopicYN="N">Atrophy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002170" MajorTopicYN="N" Type="Geographic">Canada</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004252" MajorTopicYN="N">DNA Mutational Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015342" MajorTopicYN="N">DNA Probes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003704" MajorTopicYN="N">Dementia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000939" MajorTopicYN="N">Epitopes</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005192" MajorTopicYN="N">Family Health</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005602" MajorTopicYN="N" Type="Geographic">France</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005625" MajorTopicYN="N">Frontal Lobe</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</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="N">chemistry</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010296" MajorTopicYN="N">Parietal Lobe</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010375" MajorTopicYN="N">Pedigree</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017354" MajorTopicYN="Y">Point Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016133" MajorTopicYN="N">Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015183" MajorTopicYN="N">Restriction Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012995" MajorTopicYN="N">Solubility</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013702" MajorTopicYN="N">Temporal Lobe</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>4</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>4</Month><Day>28</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>4</Month><Day>28</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10218629</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Crowther, R A" sort="Crowther, R A" uniqKey="Crowther R" first="R A" last="Crowther">R A Crowther</name><name sortKey="Gearing, M" sort="Gearing, M" uniqKey="Gearing M" first="M" last="Gearing">M. Gearing</name><name sortKey="Ghetti, B" sort="Ghetti, B" uniqKey="Ghetti B" first="B" last="Ghetti">B. Ghetti</name><name sortKey="Goedert, M" sort="Goedert, M" uniqKey="Goedert M" first="M" last="Goedert">M. Goedert</name><name sortKey="Green, J" sort="Green, J" uniqKey="Green J" first="J" last="Green">J. Green</name><name sortKey="Jones, R" sort="Jones, R" uniqKey="Jones R" first="R" last="Jones">R. Jones</name><name sortKey="Levey, A I" sort="Levey, A I" uniqKey="Levey A" first="A I" last="Levey">A I Levey</name><name sortKey="Murrell, J R" sort="Murrell, J R" uniqKey="Murrell J" first="J R" last="Murrell">J R Murrell</name><name sortKey="Schmidt, M L" sort="Schmidt, M L" uniqKey="Schmidt M" first="M L" last="Schmidt">M L Schmidt</name><name sortKey="Shoffner, J M" sort="Shoffner, J M" uniqKey="Shoffner J" first="J M" last="Shoffner">J M Shoffner</name><name sortKey="Spillantini, M G" sort="Spillantini, M G" uniqKey="Spillantini M" first="M G" last="Spillantini">M G Spillantini</name><name sortKey="Trojanowski, J Q" sort="Trojanowski, J Q" uniqKey="Trojanowski J" first="J Q" last="Trojanowski">J Q Trojanowski</name><name sortKey="Wainer, B H" sort="Wainer, B H" uniqKey="Wainer B" first="B H" last="Wainer">B H Wainer</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Mirra, S S" sort="Mirra, S S" uniqKey="Mirra S" first="S S" last="Mirra">S S Mirra</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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