Dementia in Parkinson's disease: biochemical evidence for cortical involvement using the immunodetection of abnormal Tau proteins.
Identifieur interne : 001D76 ( Ncbi/Checkpoint ); précédent : 001D75; suivant : 001D77Dementia in Parkinson's disease: biochemical evidence for cortical involvement using the immunodetection of abnormal Tau proteins.
Auteurs : P. Vermersch [France] ; A. Delacourte ; F. Javoy-Agid ; J J Hauw ; Yves Agid [France]Source :
- Annals of neurology [ 0364-5134 ] ; 1993.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Alzheimer Disease (pathology), Blotting, Western, Cerebral Cortex (pathology), Dementia (complications), Dementia (pathology), Humans, Occipital Lobe (pathology), Organ Specificity, Parkinson Disease (complications), Parkinson Disease (pathology), tau Proteins (analysis).
- MESH :
- chemical , analysis : tau Proteins.
- complications : Dementia, Parkinson Disease.
- pathology : Alzheimer Disease, Cerebral Cortex, Dementia, Occipital Lobe, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Blotting, Western, Humans, Organ Specificity.
Abstract
In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti-paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55, 64, and 69, which are known to be specific and reliable biochemical markers of Alzheimer-type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer-type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.
DOI: 10.1002/ana.410330506
PubMed: 8498822
Affiliations:
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Javoy-Agid</name></author><author><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J J" last="Hauw">J J Hauw</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8498822</idno><idno type="pmid">8498822</idno><idno type="doi">10.1002/ana.410330506</idno><idno type="wicri:Area/PubMed/Corpus">001714</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001714</idno><idno type="wicri:Area/PubMed/Curation">001673</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001673</idno><idno type="wicri:Area/PubMed/Checkpoint">001673</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001673</idno><idno type="wicri:Area/Ncbi/Merge">001D76</idno><idno type="wicri:Area/Ncbi/Curation">001D76</idno><idno type="wicri:Area/Ncbi/Checkpoint">001D76</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dementia in Parkinson's disease: biochemical evidence for cortical involvement using the immunodetection of abnormal Tau proteins.</title><author><name sortKey="Vermersch, P" sort="Vermersch, P" uniqKey="Vermersch P" first="P" last="Vermersch">P. Vermersch</name><affiliation wicri:level="3"><nlm:affiliation>Unité INSERM 156, Lille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité INSERM 156, 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="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name></author><author><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name></author><author><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J J" last="Hauw">J J Hauw</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author></analytic><series><title level="j">Annals of neurology</title><idno type="ISSN">0364-5134</idno><imprint><date when="1993" type="published">1993</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>Alzheimer Disease (pathology)</term><term>Blotting, Western</term><term>Cerebral Cortex (pathology)</term><term>Dementia (complications)</term><term>Dementia (pathology)</term><term>Humans</term><term>Occipital Lobe (pathology)</term><term>Organ Specificity</term><term>Parkinson Disease (complications)</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" qualifier="complications" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Cerebral Cortex</term><term>Dementia</term><term>Occipital Lobe</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>Blotting, Western</term><term>Humans</term><term>Organ Specificity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti-paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55, 64, and 69, which are known to be specific and reliable biochemical markers of Alzheimer-type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer-type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Hauts-de-France</li><li>Nord-Pas-de-Calais</li><li>Île-de-France</li></region><settlement><li>Lille</li><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><noCountry><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J J" last="Hauw">J J Hauw</name><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name></noCountry><country name="France"><region name="Hauts-de-France"><name sortKey="Vermersch, P" sort="Vermersch, P" uniqKey="Vermersch P" first="P" last="Vermersch">P. Vermersch</name></region><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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