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Movement Disorders

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

Authors

  • Frank L. Mastaglia MD, FRCP, FRACP,

    Corresponding author
    1. Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute Department of Medicine, University of Western Australia, Perth, Australia
    2. Department of Neurology and Clinical Neurophysiology, QEII Medical Centre, Nedlands, Western Australia, Australia
    • Centre for Neuromuscular and Neurological Disorders, 4th Floor, A Block, Queen Elizabeth II Medical Centre, Nedlands, WA 6009, Australia
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  • Russell D. Johnsen BSc,

    1. Department of Neuropathology, Royal Perth Hospital, Perth, Australia
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  • Michelle L. Byrnes PhD,

    1. Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute Department of Medicine, University of Western Australia, Perth, Australia
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  • Byron A. Kakulas AO, MD, FRACP, FRCPath

    1. Department of Neuropathology, Royal Perth Hospital, Perth, Australia
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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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