Session Information
Date: Monday, October 8, 2018
Session Title: Parkinson's Disease: Neuroimaging And Neurophysiology
Session Time: 1:15pm-2:45pm
Location: Hall 3FG
Objective: To determine whether amyloid deposition, as assessed by PET imaging with the [18F]-Florbetapir, is related in patients with Parkinson Disease and Dementia (PDD) to demographic and clinical parameters and to assess whether regional patterns of amyloid deposition correlate with specific cognitive features.
Background: The biological basis for dementia in PD appears to be multifactorial. Although cortical Lewy bodies are the most robust correlate, the comorbid Alzheimer’s Disease (AD) pathology has been also associated with PDD (1). The clinical and pathogenetic significance of amyloid deposits (Aß) in PD remains still a topic of active investigation as well as its role in the latency of dementia onset.
Methods: 21 subjects with PDD underwent standardized neurologic and neuropsychological examinations and florbetapir [18F] imaging with PET. The amyloid load was estimated on qualitative and semi-quantitative reading. Voxel-wise standardized uptake value ratio (SUVr) images were calculated using the whole cerebellum as a reference region.
Results: 8 of the 21 PDD subjects were rated as Aß+ in the visual assessment. Three more patients were categorized as Aß+ according to semi-quantitative measurements. Aß+ patients showed a more rapid cognitive decline (yearly MMSE point loss of 3,15 versus 1,12 in the Aß- group, p=0,007) and a poorer performance in the digit span forward (p=0,001) and phonemic verbal test fluency (p=0,018). No other significant group differences in demographic and clinical variables were observed. Comparing the two groups, increased Aß cortical binding was found in the frontal pole, cingulate and paracingulate gyri, precuneus, temporal and lateral occipital cortices.
Conclusions: Aß PET imaging could be able to detect a distinct category of PDD patients, with a faster progression of dementia and a different cognitive profile (2). The alpha-synuclein could promote amyloid deposition in selective brain regions, modifying the clinical phenotype of PDD patients. Unlike AD, in PDD subjects the amyloid load appear to be related to the severity and type of cognitive impairment.
References: 1) Irwin DJ, et al. Neuropathologic substrates of Parkinson disease dementia. Ann Neurol. 2012;72:587–98. 2) Gomperts SN. Imaging the role of amyloid in PD dementia and dementia with Lewy bodies. Curr Neurol Neurosci Rep. 2014;14(8):472.
To cite this abstract in AMA style:
G. Palermo, G. Aghakhanyan, L. Tommasini, D. Frosini, D. Volterrani, U. Bonuccelli, R. Ceravolo. A Florbetapir [F18] amyloid PET Imaging study in Parkinson’s disease Dementia (PDD): The influence of amyloid deposition on cognitive status and course of disease progression [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/a-florbetapir-f18-amyloid-pet-imaging-study-in-parkinsons-disease-dementia-pdd-the-influence-of-amyloid-deposition-on-cognitive-status-and-course-of-disease-progression/. Accessed December 9, 2024.« Back to 2018 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/a-florbetapir-f18-amyloid-pet-imaging-study-in-parkinsons-disease-dementia-pdd-the-influence-of-amyloid-deposition-on-cognitive-status-and-course-of-disease-progression/