Objective: To investigate the relationship between cerebral amyloid accumulation and cognition in Parkinson’s disease (PD).

Background: The neuropathology underlying the development of dementia in Parkinson’s disease is likely multifactorial. While the cortical spread of misfolded alpha-synuclein protein undoubtedly plays an important role, Alzheimer neuropathology, including accumulation of misfolded beta-amyloid and tau proteins, may also contribute to the emergence of dementia in PD (PDD).

Methods: Movement Disorder Society level II criteria were used to classify 110 participants with PD as having normal cognition (PDN, n=23), mild cognitive impairment (PD-MCI, n=76), or dementia (PDD, n=16). We acquired 18F-Florbetaben (FBB) amyloid PET and structural MRI in all participants. Aβ was expressed in centiloids and as standardised uptake value ratio (SUVR) using the Centiloid Project cerebellum region as reference. Amyloid deposition was assessed across cognitive groups, and for association with a continuous measure of (1) global cognitive and (2) memory performance using Bayesian regression in the following regions of interest: cortex, caudate, putamen, globus pallidus, thalamus, amygdala, hippocampus, and precuneus. Whole-brain, voxel-wise SUVR was also investigated.

Results: We identified no evidence of significant association between FBB binding and global cognition or memory function across multiple cortical and subcortical regions. Age, however, was significantly associated with cortical FBB deposition.

Conclusions: The lack of evidence for association between cognitive performance and amyloid deposition in PD suggests that amyloid accumulation is not the primary cause of cognitive impairments in most patients with PD. Dementia most likely arises as a result of alternative pathologies.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/amyloid-pet-and-cognition-in-parkinsons-disease/