Postmortem delay ranged from 4 to 12 hours. These subjects, age 80 to 90 years (mean, 85.4 years), were examined thoroughly by general pathologists and neuropathologists, and none of them were diagnosed as having had AD. Five AD cases (68-84 years; mean, 76.8 years) were neuropatho-From the
Prevalence of amyloid-β deposition in the cerebral cortex in Parkinson's disease
✍ Scribed by Frank L. Mastaglia; Russell D. Johnsen; Michelle L. Byrnes; Byron A. Kakulas
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 69 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
✦ Synopsis
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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