Distribution and Load of Amyloid-β Pathology in Parkinson Disease and Dementia with Lewy Bodies.

J Neuropathol Exp Neurol

From the Department of Anatomy and Neurosciences, Section Quantitative Morphology (DHH, DLEV, EH, WDJVDB), Department of Neurology, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands (DHH, AWL, EMJF), Netherlands Institute for Neuroscience, Amsterdam, The Netherlands (NBB) and Department of Pathology, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands (AJR).

Published: October 2016

AI Article Synopsis

  • The study compares the presence and distribution of amyloid-β (Aβ) pathology in Parkinson's disease (PD), Parkinson's disease with dementia (PDD), and Dementia with Lewy bodies (DLB).
  • DLB patients had significantly higher Aβ scores than PDD and PD patients, indicating a greater burden of this pathology.
  • Findings suggest that the varying levels of Aβ pathology may play a role in cognitive decline seen in PDD and DLB, particularly in early-stage severe dementia.

Article Abstract

Parkinson disease (PD), Parkinson disease with dementia (PDD), and Dementia with Lewy bodies (DLB) differ clinically with regard to the presence and timing of dementia. In this postmortem study, we evaluated whether the burden and distribution pattern of amyloid-β (Aβ) pathology differs among these disease entities. We assessed Aβ phases and neuritic plaque scores in 133 patients fulfilling clinical diagnostic criteria for PD, PDD, and DLB, and determined the presence and load of Aβ pathology in 5 cortical and 4 subcortical regions in a subset of patients (n = 89) using a multispectral imaging system. Aβ phases and neuritic plaque scores were higher in DLB versus PDD (both p < 0.001) and in PDD vs PD patients (p = 0.020 and 0.022, respectively). Aβ pathology was more often observed in the entorhinal cortex, amygdala and putamen in DLB versus PDD patients; Aβ load was higher in both cortical and subcortical regions. PDD patients had more frequent Aβ pathology in temporal cortex and higher Aβ load in cortical regions and striatum versus PD patients. Our findings suggest that the load and extent of Aβ pathology may contribute to cognitive dysfunction in PDD and the early-stage severe dementia in DLB.

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Source
http://dx.doi.org/10.1093/jnen/nlw070DOI Listing

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