Anatamopathological spectrum of tauopathies.
Identifieur interne : 003717 ( PubMed/Corpus ); précédent : 003716; suivant : 003718Anatamopathological spectrum of tauopathies.
Auteurs : Tamas Revesz ; Janice L. HoltonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- Brain (pathology), Dementia (genetics), Dementia (pathology), Diagnosis, Differential, Humans, Inclusion Bodies (pathology), Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (pathology), Neuroglia (pathology), Neurons (pathology), Parkinsonian Disorders (genetics), Parkinsonian Disorders (pathology), Tauopathies (genetics), Tauopathies (pathology), tau Proteins (genetics), tau Proteins (metabolism).
- MESH :
- chemical , genetics : tau Proteins.
- genetics : Dementia, Neurodegenerative Diseases, Parkinsonian Disorders, Tauopathies.
- chemical , metabolism : tau Proteins.
- pathology : Brain, Dementia, Inclusion Bodies, Neurodegenerative Diseases, Neuroglia, Neurons, Parkinsonian Disorders, Tauopathies.
- Diagnosis, Differential, Humans.
Abstract
The presence of tau-positive intraneuronal filamentous inclusions with or without additional inclusions in glial cells has been recognised as a major neuropathological feature in a significant group of neurodegenerative diseases, which are described as tauopathies. In one category of such diseases, the neuronal inclusions occur in association with extracellular deposition of a second aggregated protein (secondary tauopathies), whereas in another, the filamentous inclusions composed of tau are the sole neuropathological abnormality (primary tauopathies). Genetic studies of tauopathies in general, and in frontotemporal dementia with parkinsonism linked to chromosome 17 in particular, have significantly contributed to our knowledge about the pathogenesis not only of rare hereditary conditions but also of other more common diseases such as Alzheimer's disease and progressive supranuclear palsy.
DOI: 10.1002/mds.10558
PubMed: 14502651
Links to Exploration step
pubmed:14502651Le document en format XML
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Holton</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:14502651</idno><idno type="pmid">14502651</idno><idno type="doi">10.1002/mds.10558</idno><idno type="wicri:Area/PubMed/Corpus">003717</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Anatamopathological spectrum of tauopathies.</title><author><name sortKey="Revesz, Tamas" sort="Revesz, Tamas" uniqKey="Revesz T" first="Tamas" last="Revesz">Tamas Revesz</name><affiliation><nlm:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom. T.Revesz@ion.ucl.ac.uk</nlm:affiliation></affiliation></author><author><name sortKey="Holton, Janice L" sort="Holton, Janice L" uniqKey="Holton J" first="Janice L" last="Holton">Janice L. Holton</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (pathology)</term><term>Dementia (genetics)</term><term>Dementia (pathology)</term><term>Diagnosis, Differential</term><term>Humans</term><term>Inclusion Bodies (pathology)</term><term>Neurodegenerative Diseases (genetics)</term><term>Neurodegenerative Diseases (pathology)</term><term>Neuroglia (pathology)</term><term>Neurons (pathology)</term><term>Parkinsonian Disorders (genetics)</term><term>Parkinsonian Disorders (pathology)</term><term>Tauopathies (genetics)</term><term>Tauopathies (pathology)</term><term>tau Proteins (genetics)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dementia</term><term>Neurodegenerative Diseases</term><term>Parkinsonian Disorders</term><term>Tauopathies</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Dementia</term><term>Inclusion Bodies</term><term>Neurodegenerative Diseases</term><term>Neuroglia</term><term>Neurons</term><term>Parkinsonian Disorders</term><term>Tauopathies</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Diagnosis, Differential</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The presence of tau-positive intraneuronal filamentous inclusions with or without additional inclusions in glial cells has been recognised as a major neuropathological feature in a significant group of neurodegenerative diseases, which are described as tauopathies. In one category of such diseases, the neuronal inclusions occur in association with extracellular deposition of a second aggregated protein (secondary tauopathies), whereas in another, the filamentous inclusions composed of tau are the sole neuropathological abnormality (primary tauopathies). Genetic studies of tauopathies in general, and in frontotemporal dementia with parkinsonism linked to chromosome 17 in particular, have significantly contributed to our knowledge about the pathogenesis not only of rare hereditary conditions but also of other more common diseases such as Alzheimer's disease and progressive supranuclear palsy.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">14502651</PMID><DateCreated><Year>2003</Year><Month>09</Month><Day>22</Day></DateCreated><DateCompleted><Year>2004</Year><Month>02</Month><Day>24</Day></DateCompleted><DateRevised><Year>2004</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>18 Suppl 6</Volume><PubDate><Year>2003</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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Genetic studies of tauopathies in general, and in frontotemporal dementia with parkinsonism linked to chromosome 17 in particular, have significantly contributed to our knowledge about the pathogenesis not only of rare hereditary conditions but also of other more common diseases such as Alzheimer's disease and progressive supranuclear palsy.</AbstractText><CopyrightInformation>Copyright 2003 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Revesz</LastName><ForeName>Tamas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom. 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