Dementia in idiopathic Parkinson's disease
Identifieur interne : 000325 ( France/Analysis ); précédent : 000324; suivant : 000326Dementia in idiopathic Parkinson's disease
Auteurs : P. Gaspar [France] ; F. Gray [France]Source :
- Acta Neuropathologica [ 0001-6322 ] ; 1984-03-01.
Abstract
Summary: Neuronal loss was estimated semiquantitatively in the substantia nigra (SN) and locus coeruleus (LC), and by cell counts in the nucleus basalis of Meynert (NBM), in 32 patients with idiopathic Parkinson's disease (14 non-demented and 18 demented). The number of senile plaques (SP) and neurofibrillary tangles (NFT) was rated in four cortical areas. Neuronal loss in the SN seemed in dependent of mental impairment, while severe lesions of the LC were more frequent in demented patients. In the NBM, neuronal loss and Lewy bodies were observed in most cases (95%) and were associated with significant reductions of choline acetyltransferase (CAT) activity both in the NBM and the cortex (measurements available for 13 cases). This confirms that the cholinergic innominatocortical pathway is damaged in Parkinson's disease and that the lesion is severer in subjects with dementia. SP and NFT were present in the cortex in 75% of the cases and significantly more numerous in demented patients. However, in 37% of the cases (six cases with dementia), the score for cortical changes was low and could be related to age. Cortical SP and NFT were not correlated to the degree of cell loss in LC and NBM, or to CAT activity in the cortex or NBM. Damage to coeruleocortical, innominato-cortical and intra-cortical neurones could each play a role in the appearance of dementia in Parkinsonism. The lesions in the different neuronal systems do not seem to evolve in parallel, but may be additive or potentiate one another in terms of functional expression. Also, the variety in extent and degree of lesions encountered in Parkinson's disease may offer a pathological substrate for the wide variety of mental symptoms described in this illness.
Url:
DOI: 10.1007/BF00695605
Affiliations:
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Gray</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F30DEFA75B1CB15AB31E708E4A252D424B626DA3</idno><date when="1984" year="1984">1984</date><idno type="doi">10.1007/BF00695605</idno><idno type="url">https://api.istex.fr/document/F30DEFA75B1CB15AB31E708E4A252D424B626DA3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000548</idno><idno type="wicri:Area/Main/Curation">000474</idno><idno type="wicri:Area/Main/Exploration">002A57</idno><idno type="wicri:Area/France/Extraction">000325</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Dementia in idiopathic Parkinson's disease</title><author><name sortKey="Gaspar, P" sort="Gaspar, P" uniqKey="Gaspar P" first="P." last="Gaspar">P. Gaspar</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 47, Bd. de l'Hôpital, F-75651, Paris Cédex 13</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris Cédex 13</settlement></placeName></affiliation></author><author><name sortKey="Gray, F" sort="Gray, F" uniqKey="Gray F" first="F." last="Gray">F. Gray</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neuropathologie Charles Foix, Hôpital de la Salpêtrière, 47, Bd. de l'Hôpital, F-75651, Paris Cédex 13</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris Cédex 13</settlement></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neuropathologica</title><title level="j" type="abbrev">Acta Neuropathol</title><idno type="ISSN">0001-6322</idno><idno type="eISSN">1432-0533</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1984-03-01">1984-03-01</date><biblScope unit="volume">64</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="43">43</biblScope><biblScope unit="page" to="52">52</biblScope></imprint><idno type="ISSN">0001-6322</idno></series><idno type="istex">F30DEFA75B1CB15AB31E708E4A252D424B626DA3</idno><idno type="DOI">10.1007/BF00695605</idno><idno type="ArticleID">Art8</idno><idno type="ArticleID">BF00695605</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6322</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Neuronal loss was estimated semiquantitatively in the substantia nigra (SN) and locus coeruleus (LC), and by cell counts in the nucleus basalis of Meynert (NBM), in 32 patients with idiopathic Parkinson's disease (14 non-demented and 18 demented). The number of senile plaques (SP) and neurofibrillary tangles (NFT) was rated in four cortical areas. Neuronal loss in the SN seemed in dependent of mental impairment, while severe lesions of the LC were more frequent in demented patients. In the NBM, neuronal loss and Lewy bodies were observed in most cases (95%) and were associated with significant reductions of choline acetyltransferase (CAT) activity both in the NBM and the cortex (measurements available for 13 cases). This confirms that the cholinergic innominatocortical pathway is damaged in Parkinson's disease and that the lesion is severer in subjects with dementia. SP and NFT were present in the cortex in 75% of the cases and significantly more numerous in demented patients. However, in 37% of the cases (six cases with dementia), the score for cortical changes was low and could be related to age. Cortical SP and NFT were not correlated to the degree of cell loss in LC and NBM, or to CAT activity in the cortex or NBM. Damage to coeruleocortical, innominato-cortical and intra-cortical neurones could each play a role in the appearance of dementia in Parkinsonism. The lesions in the different neuronal systems do not seem to evolve in parallel, but may be additive or potentiate one another in terms of functional expression. Also, the variety in extent and degree of lesions encountered in Parkinson's disease may offer a pathological substrate for the wide variety of mental symptoms described in this illness.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris Cédex 13</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Gaspar, P" sort="Gaspar, P" uniqKey="Gaspar P" first="P." last="Gaspar">P. Gaspar</name></region><name sortKey="Gray, F" sort="Gray, F" uniqKey="Gray F" first="F." last="Gray">F. 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