Prevalence of amyloid‐β deposition in the cerebral cortex in Parkinson's disease
Identifieur interne : 001721 ( Main/Exploration ); précédent : 001720; suivant : 001722Prevalence of amyloid‐β deposition in the cerebral cortex in Parkinson's disease
Auteurs : Frank L. Mastaglia [Australie] ; Russell D. Johnsen [Australie] ; Michelle L. Byrnes [Australie] ; Byron A. Kakulas [Australie]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-01.
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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.
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DOI: 10.1002/mds.10295
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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. 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