Neurofibrillary tangle parkinsonian disorders--tau pathology and tau genetics.
Identifieur interne : 004163 ( PubMed/Checkpoint ); précédent : 004162; suivant : 004164Neurofibrillary tangle parkinsonian disorders--tau pathology and tau genetics.
Auteurs : H R Morris [Royaume-Uni] ; A J Lees ; N W WoodSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1999.
English descriptors
- KwdEn :
- Brain (metabolism), Brain (pathology), Chromosome Aberrations (genetics), Chromosome Disorders, Chromosomes, Human, Pair 17 (genetics), Dementia (genetics), Genes (genetics), Humans, Neurofibrillary Tangles (genetics), Neurofibrillary Tangles (metabolism), Parkinsonian Disorders (genetics), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Point Mutation (genetics), tau Proteins (genetics), tau Proteins (metabolism).
- MESH :
- chemical , genetics : tau Proteins.
- genetics : Chromosome Aberrations, Chromosomes, Human, Pair 17, Dementia, Genes, Neurofibrillary Tangles, Parkinsonian Disorders, Point Mutation.
- metabolism : Brain, Neurofibrillary Tangles, Parkinsonian Disorders, tau Proteins.
- pathology : Brain, Parkinsonian Disorders.
- Chromosome Disorders, Humans.
Abstract
A number of related conditions, including progressive supranuclear palsy (PSP), corticobasal degeneration, Pick's disease, and the parkinsonism dementia complex of Guam, are characterized by the deposition of tau neurofibrillary tangles in the absence of amyloid pathology. These diseases share some overlap in their topography and clinical features but can be subdivided into three main groups according to the isoforms of the alternatively spliced tau gene that are deposited. The recent description of mutation in tau in frontotemporal dementia, and a common variant of tau that predisposes to PSP, and the relationship of these changes to the tau protein subgroups offers new insights into the pathogenesis of these disorders.
PubMed: 10495033
Affiliations:
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These diseases share some overlap in their topography and clinical features but can be subdivided into three main groups according to the isoforms of the alternatively spliced tau gene that are deposited. The recent description of mutation in tau in frontotemporal dementia, and a common variant of tau that predisposes to PSP, and the relationship of these changes to the tau protein subgroups offers new insights into the pathogenesis of these disorders.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">10495033</PMID><DateCreated><Year>1999</Year><Month>11</Month><Day>10</Day></DateCreated><DateCompleted><Year>1999</Year><Month>11</Month><Day>10</Day></DateCompleted><DateRevised><Year>2014</Year><Month>02</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>14</Volume><Issue>5</Issue><PubDate><Year>1999</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neurofibrillary tangle parkinsonian disorders--tau pathology and tau genetics.</ArticleTitle><Pagination><MedlinePgn>731-6</MedlinePgn></Pagination><Abstract><AbstractText>A number of related conditions, including progressive supranuclear palsy (PSP), corticobasal degeneration, Pick's disease, and the parkinsonism dementia complex of Guam, are characterized by the deposition of tau neurofibrillary tangles in the absence of amyloid pathology. These diseases share some overlap in their topography and clinical features but can be subdivided into three main groups according to the isoforms of the alternatively spliced tau gene that are deposited. The recent description of mutation in tau in frontotemporal dementia, and a common variant of tau that predisposes to PSP, and the relationship of these changes to the tau protein subgroups offers new insights into the pathogenesis of these disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morris</LastName><ForeName>H R</ForeName><Initials>HR</Initials><AffiliationInfo><Affiliation>University Department of Clinical Neurology, Institute of Neurology, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lees</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Wood</LastName><ForeName>N W</ForeName><Initials>NW</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G9810900</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002869">Chromosome Aberrations</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D025063">Chromosome Disorders</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002886">Chromosomes, Human, Pair 17</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003704">Dementia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005796">Genes</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016874">Neurofibrillary Tangles</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017354">Point Mutation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016875">tau Proteins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>48</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>9</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>9</Month><Day>24</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>9</Month><Day>24</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10495033</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><noCountry><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name><name sortKey="Wood, N W" sort="Wood, N W" uniqKey="Wood N" first="N W" last="Wood">N W Wood</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Morris, H R" sort="Morris, H R" uniqKey="Morris H" first="H R" last="Morris">H R Morris</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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