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Brain amyloid contribution to cognitive dysfunction in Lewy bodies disorders: a pilot study

R. Biundo, E. Fiorenzato, D. Cecchin, C. Salvotti, L. Weis, A. Antonini (Venice, Italy)

Meeting: 2019 International Congress

Abstract Number: 1664

Keywords: Cognitive dysfunction, Dementia with Lewy bodies (DLB), Positron emission tomography(PET)

Session Information

Date: Wednesday, September 25, 2019

Session Title: Cognition and Cognitive Disorders

Session Time: 1:15pm-2:45pm

Location: Agora 3 East, Level 3

Objective: To investigate regional [18F]florbetapir binding to amyloid-β and its contribution to cognitive dysfunction in Lewy bodies disorders.

Background: Lewy bodies disorders like Parkinson’s disease dementia (PDD) and dementia with Lewy Bodies (DLB) are synucleopathies but accumulation of beta amyloid (Aβ) has been frequently reported [1, 2]. Clarifying the relationships of Aβ and α-syn in LBD may yield insights on the contributions of comorbid Alzheimer’s disease (AD) pathology to dementia progression.

Method: Four DLB, 16 PD [3 PD with normal cognition, 7 PD with mild cognitive impairment, 6 PDD] underwent [18F]florbetapir positron emission tomography (PET) scanning. Clinical features, including demographic characteristics, motor severity and cognitive testing were assessed. For the purpose of this study, we analyzed various neuropsychological tests assessing all cognitive functions and allowing Level II cognitive diagnosis.

Results: There were 7/20 (35%) amyloid positive (Aβ +) patients at visual assessment. We found that Aβ+  had worse performance than Aβ- patients on global cognition, as assessed by Montreal Cognitive Assessment (MoCA) (p = 0.024) and in the memory domain (Word Paired Associated Test) (p =0.037). There was a tendency for a poorer performance in  visuospatial and executive domains (assessed with the incomplete letters of Visual Object and Space Perception and Stroop test) (p = 0.087 and p = 0.068, respectively).

Conclusion: Our results corroborate evidence of additional Aβ contribution to worse global cognitive profile in Lewy Body disorders [3] and to verbal memory abilities. These findings support the therapeutic potential of anti-Aβ interventions in patients with Lewy Body Dementia with positive [18F]florbetapir PET.

References: 1. Petrou M, Dwamena BA, Foerster BR, MacEachern MP, Bohnen NI, Muller ML, Albin RL, Frey KA (2015) Amyloid deposition in Parkinson’s disease and cognitive impairment: a systematic review. Mov Disord 30:928-935 2. Gomperts SN, Rentz DM, Moran E, Becker JA, Locascio JJ, Klunk WE, Mathis CA, Elmaleh DR, Shoup T, Fischman AJ, Hyman BT, Growdon JH, Johnson KA (2008) Imaging amyloid deposition in Lewy body diseases. Neurology 71:903-910 3. Fiorenzato E, Biundo R, Cecchin D, Frigo AC, Kim J, Weis L, Strafella AP, Antonini A, Cagnin A (2018) Brain Amyloid Contribution to Cognitive Dysfunction in Early-Stage Parkinson’s Disease: The PPMI Dataset. Journal of Alzheimer’s Disease 66:229-237

To cite this abstract in AMA style:

R. Biundo, E. Fiorenzato, D. Cecchin, C. Salvotti, L. Weis, A. Antonini. Brain amyloid contribution to cognitive dysfunction in Lewy bodies disorders: a pilot study [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/brain-amyloid-contribution-to-cognitive-dysfunction-in-lewy-bodies-disorders-a-pilot-study/. Accessed June 14, 2025.
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