Amyloid beta-peptide and the dementia of Parkinson's disease.
Identifieur interne : 004C18 ( Ncbi/Checkpoint ); précédent : 004C17; suivant : 004C19Amyloid beta-peptide and the dementia of Parkinson's disease.
Auteurs : K. Jendroska [Allemagne] ; A J Lees ; Werner Poewe [Autriche] ; S E DanielSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1996.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (pathology), Amyloid beta-Peptides (analysis), Brain (pathology), Cerebral Cortex (pathology), Dementia (pathology), Diagnosis, Differential, Female, Humans, Image Processing, Computer-Assisted, Lewy Bodies (pathology), Male, Middle Aged, Neurofibrillary Tangles (pathology), Parkinson Disease (pathology), Reference Values.
- MESH :
- chemical , analysis : Amyloid beta-Peptides.
- pathology : Alzheimer Disease, Brain, Cerebral Cortex, Dementia, Lewy Bodies, Neurofibrillary Tangles, Parkinson Disease.
- Aged, Aged, 80 and over, Diagnosis, Differential, Female, Humans, Image Processing, Computer-Assisted, Male, Middle Aged, Reference Values.
Abstract
It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to "early" Alzheimer-type pathology. To determine whether amyloid beta-peptide (A beta) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for A beta. Twenty-three cases with PD had dementia, including all nine with A beta distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable A beta accumulation were not demented. Neither AD nor A beta deposition was increased in PD, furthermore, there was no statistical correlation between the amount of A beta and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to A beta, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or "early" Alzheimer-type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.
DOI: 10.1002/mds.870110609
PubMed: 8914090
Affiliations:
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Jendroska</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, Charité, Berlin, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, Charité, Berlin</wicri:regionArea><placeName><region type="land" nuts="3">Berlin</region><settlement type="city">Berlin</settlement></placeName></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author><author><name sortKey="Poewe, W" sort="Poewe, W" uniqKey="Poewe W" first="W" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8914090</idno><idno type="pmid">8914090</idno><idno type="doi">10.1002/mds.870110609</idno><idno type="wicri:Area/PubMed/Corpus">004764</idno><idno type="wicri:Area/PubMed/Curation">004764</idno><idno type="wicri:Area/PubMed/Checkpoint">004879</idno><idno type="wicri:Area/Ncbi/Merge">004C18</idno><idno type="wicri:Area/Ncbi/Curation">004C18</idno><idno type="wicri:Area/Ncbi/Checkpoint">004C18</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Amyloid beta-peptide and the dementia of Parkinson's disease.</title><author><name sortKey="Jendroska, K" sort="Jendroska, K" uniqKey="Jendroska K" first="K" last="Jendroska">K. Jendroska</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, Charité, Berlin, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, Charité, Berlin</wicri:regionArea><placeName><region type="land" nuts="3">Berlin</region><settlement type="city">Berlin</settlement></placeName></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author><author><name sortKey="Poewe, W" sort="Poewe, W" uniqKey="Poewe W" first="W" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</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="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (pathology)</term><term>Amyloid beta-Peptides (analysis)</term><term>Brain (pathology)</term><term>Cerebral Cortex (pathology)</term><term>Dementia (pathology)</term><term>Diagnosis, Differential</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Lewy Bodies (pathology)</term><term>Male</term><term>Middle Aged</term><term>Neurofibrillary Tangles (pathology)</term><term>Parkinson Disease (pathology)</term><term>Reference Values</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Amyloid beta-Peptides</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term><term>Cerebral Cortex</term><term>Dementia</term><term>Lewy Bodies</term><term>Neurofibrillary Tangles</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Diagnosis, Differential</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Male</term><term>Middle Aged</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to "early" Alzheimer-type pathology. To determine whether amyloid beta-peptide (A beta) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for A beta. Twenty-three cases with PD had dementia, including all nine with A beta distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable A beta accumulation were not demented. Neither AD nor A beta deposition was increased in PD, furthermore, there was no statistical correlation between the amount of A beta and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to A beta, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or "early" Alzheimer-type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Autriche</li></country><region><li>Berlin</li><li>Tyrol (Land)</li></region><settlement><li>Berlin</li><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><noCountry><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</name><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></noCountry><country name="Allemagne"><region name="Berlin"><name sortKey="Jendroska, K" sort="Jendroska, K" uniqKey="Jendroska K" first="K" last="Jendroska">K. Jendroska</name></region></country><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, W" sort="Poewe, W" uniqKey="Poewe W" first="W" last="Poewe">Werner Poewe</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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