MovDisordV3, PascalFrancis, Corpus, bibRecord, 002558

Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease

Identifieur interne : 002558 ( PascalFrancis/Corpus ); précédent : 002557; suivant : 002559

Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease

Auteurs : Frank L. Mastaglia ; Russell D. Johnsen ; Michelle L. Byrnes ; Byron A. Kakulas

Source :

Movement disorders [ 0885-3185 ] ; 2003.

RBID : Pascal:03-0146648

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Cortex cérébral, Vaisseau sanguin, Protéine amyloïde β, Démence, Anatomopathologie, Exploration, Complication, Adulte.

English descriptors

KwdEn :
- Adult, Blood vessel, Cerebral cortex, Complication, Dementia, Exploration, Parkinson disease, Pathology, β Amyloid protein.

Abstract

The pathological basis for the dementia which occurs in 20 to 40% of patients with idiopathic Parkinson's disease (PD) remains uncertain. In the present postmortem study, we compared the prevalence and severity of parenchymal and vascular amyloid-β (Aβ) deposition in the cerebral cortex in a group of 57 PD brains, including 13 cases with dementia, and in 100 control brains. A higher proportion of PD brains had vascular Aβ deposition, whereas the proportions and severity of parenchymal Aβ were similar in the PD and control groups. There was a poor correlation between Aβ deposition and neurofibrillary tangles which were present in only small numbers in a minority of cases. Cortical Aβ deposition was present in only 6 of the 13 cases with dementia and only 3 fulfilled the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria for definite Alzheimer's disease. The present findings confirm that dementia in PD is only infrequently due to fully established Alzheimer's disease. However, vascular and parenchymal Aβ deposition could still contribute to dementia and cognitive decline when combined with other changes such as α-synuclein deposition in the cerebral cortex and cortical Lewy bodies.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 03-0146648 INIST
ET :	Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease
AU :	MASTAGLIA (Frank L.); JOHNSEN (Russell D.); BYRNES (Michelle L.); KAKULAS (Byron A.)
AF :	Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute, and Department of Medicine, University of Western Australia/Perth/Australie (1 aut., 3 aut.); Department of Neurology and Clinical Neurophysiology, QEII Medical Centre/Nedlands, Western Australia/Australie (1 aut.); Department of Neuropathology, Royal Perth Hospital/Perth/Australie (2 aut., 4 aut.)
DT :	Publication en série; Courte communication, note brève; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2003; Vol. 18; No. 1; Pp. 81-86; Bibl. 50 ref.
LA :	Anglais
EA :	The pathological basis for the dementia which occurs in 20 to 40% of patients with idiopathic Parkinson's disease (PD) remains uncertain. In the present postmortem study, we compared the prevalence and severity of parenchymal and vascular amyloid-β (Aβ) deposition in the cerebral cortex in a group of 57 PD brains, including 13 cases with dementia, and in 100 control brains. A higher proportion of PD brains had vascular Aβ deposition, whereas the proportions and severity of parenchymal Aβ were similar in the PD and control groups. There was a poor correlation between Aβ deposition and neurofibrillary tangles which were present in only small numbers in a minority of cases. Cortical Aβ deposition was present in only 6 of the 13 cases with dementia and only 3 fulfilled the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria for definite Alzheimer's disease. The present findings confirm that dementia in PD is only infrequently due to fully established Alzheimer's disease. However, vascular and parenchymal Aβ deposition could still contribute to dementia and cognitive decline when combined with other changes such as α-synuclein deposition in the cerebral cortex and cortical Lewy bodies.
CC :	002B17G; 235
FD :	Parkinson maladie; Cortex cérébral; Vaisseau sanguin; Protéine amyloïde β; Démence; Anatomopathologie; Exploration; Complication; Adulte
FG :	Homme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Appareil circulatoire; Trouble neurologique
ED :	Parkinson disease; Cerebral cortex; Blood vessel; β Amyloid protein; Dementia; Pathology; Exploration; Complication; Adult
EG :	Human; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Circulatory system; Neurological disorder
SD :	Parkinson enfermedad; Corteza cerebral; Vaso sanguíneo; Proteína amiloide β; Demencia; Anatomía patológica; Exploración; Complicación; Adulto
LO :	INIST-20953.354000103916060080
ID :	03-0146648

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Pascal:03-0146648

Le document en format XML

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<front><div type="abstract" xml:lang="en">The pathological basis for the dementia which occurs in 20 to 40% of patients with idiopathic Parkinson's disease (PD) remains uncertain. In the present postmortem study, we compared the prevalence and severity of parenchymal and vascular amyloid-β (Aβ) deposition in the cerebral cortex in a group of 57 PD brains, including 13 cases with dementia, and in 100 control brains. A higher proportion of PD brains had vascular Aβ deposition, whereas the proportions and severity of parenchymal Aβ were similar in the PD and control groups. There was a poor correlation between Aβ deposition and neurofibrillary tangles which were present in only small numbers in a minority of cases. Cortical Aβ deposition was present in only 6 of the 13 cases with dementia and only 3 fulfilled the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria for definite Alzheimer's disease. The present findings confirm that dementia in PD is only infrequently due to fully established Alzheimer's disease. However, vascular and parenchymal Aβ deposition could still contribute to dementia and cognitive decline when combined with other changes such as α-synuclein deposition in the cerebral cortex and cortical Lewy bodies.</div>
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<server><NO>PASCAL 03-0146648 INIST</NO>
<ET>Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease</ET>
<AU>MASTAGLIA (Frank L.); JOHNSEN (Russell D.); BYRNES (Michelle L.); KAKULAS (Byron A.)</AU>
<AF>Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute, and Department of Medicine, University of Western Australia/Perth/Australie (1 aut., 3 aut.); Department of Neurology and Clinical Neurophysiology, QEII Medical Centre/Nedlands, Western Australia/Australie (1 aut.); Department of Neuropathology, Royal Perth Hospital/Perth/Australie (2 aut., 4 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2003; Vol. 18; No. 1; Pp. 81-86; Bibl. 50 ref.</SO>
<LA>Anglais</LA>
<EA>The pathological basis for the dementia which occurs in 20 to 40% of patients with idiopathic Parkinson's disease (PD) remains uncertain. In the present postmortem study, we compared the prevalence and severity of parenchymal and vascular amyloid-β (Aβ) deposition in the cerebral cortex in a group of 57 PD brains, including 13 cases with dementia, and in 100 control brains. A higher proportion of PD brains had vascular Aβ deposition, whereas the proportions and severity of parenchymal Aβ were similar in the PD and control groups. There was a poor correlation between Aβ deposition and neurofibrillary tangles which were present in only small numbers in a minority of cases. Cortical Aβ deposition was present in only 6 of the 13 cases with dementia and only 3 fulfilled the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria for definite Alzheimer's disease. The present findings confirm that dementia in PD is only infrequently due to fully established Alzheimer's disease. However, vascular and parenchymal Aβ deposition could still contribute to dementia and cognitive decline when combined with other changes such as α-synuclein deposition in the cerebral cortex and cortical Lewy bodies.</EA>
<CC>002B17G; 235</CC>
<FD>Parkinson maladie; Cortex cérébral; Vaisseau sanguin; Protéine amyloïde β; Démence; Anatomopathologie; Exploration; Complication; Adulte</FD>
<FG>Homme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Appareil circulatoire; Trouble neurologique</FG>
<ED>Parkinson disease; Cerebral cortex; Blood vessel; β Amyloid protein; Dementia; Pathology; Exploration; Complication; Adult</ED>
<EG>Human; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Circulatory system; Neurological disorder</EG>
<SD>Parkinson enfermedad; Corteza cerebral; Vaso sanguíneo; Proteína amiloide β; Demencia; Anatomía patológica; Exploración; Complicación; Adulto</SD>
<LO>INIST-20953.354000103916060080</LO>
<ID>03-0146648</ID>
</server>
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Movement Disorders (revue)

Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease

Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease

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