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Quantification of Brain β-Amyloid Load in Parkinson's Disease With Mild Cognitive Impairment: A PET/MRI Study
Michela Garon1, Luca Weis1, Eleonora Fiorenzato2
1Parkinson and Movement Disorders Unit, Department of Neuroscience, University of Padua, Padua, Italy.
Background:
Mild cognitive impairment in Parkinson's disease (PD-MCI) is associated with faster cognitive decline and conversion to dementia. There is uncertainty about the role of β-amyloid (Aβ) co-pathology and its contribution to the variability in PD-MCI profile and cognitive progression.
Objective:
To study how presence of Aβ affects clinical and cognitive manifestations as well as regional brain volumes in PD-MCI.
Methods:
Twenty-five PD-MCI patients underwent simultaneous PET/3T-MRI with [18F]flutemetamol and a clinical and neuropsychological examination allowing level II diagnosis. We tested pairwise differences in motor, clinical, and cognitive features with Mann-Whitney U test. We calculated [18F]flutemetamol (FMM) standardized uptake value ratios (SUVR) in striatal and cortical ROIs, and we performed a univariate linear regression analysis between the affected cognitive domains and the mean SUVR. Finally, we investigated differences in cortical and subcortical brain regional volumes with magnetic resonance imaging (MRI).
Results:
There were 8 Aβ+ and 17 Aβ- PD-MCI. They did not differ for age, disease duration, clinical, motor, behavioral, and global cognition scores. PD-MCI-Aβ+ showed worse performance in the overall executive domain (p = 0.037). Subcortical ROIs analysis showed significant Aβ deposition in PD-MCI-Aβ+ patients in the right caudal and rostral middle frontal cortex, in precuneus, in left paracentral and pars triangularis (p < 0.0001), and bilaterally in the putamen (p = 0.038). Cortical regions with higher amyloid load correlated with worse executive performances (p < 0.05). Voxel-based morphometry (VBM) analyses showed no between groups differences.
Conclusions:
Presence of cerebral Aβ worsens executive functions, but not motor and global cognitive abilities in PD-MCI, and it is not associated with middle-temporal cortex atrophy. These findings, together with the observation of significant proportion of PD-MCI-Aβ-, suggest that Aβ may not be the main pathogenetic determinant of cognitive deterioration in PD-MCI, but it would rather aggravate deficits in domains vulnerable to Parkinson primary pathology.
Insights
Beta-amyloid (Aβ) presence worsens executive functions in Parkinson's disease with mild cognitive impairment (PD-MCI). However, Aβ does not impact motor skills or overall cognition, suggesting it aggravates existing deficits rather than being the primary cause.
Area of Science:
- Neuroscience
- Neurology
- Medical Imaging
Background:
- Mild cognitive impairment in Parkinson's disease (PD-MCI) is linked to accelerated cognitive decline and dementia.
- The specific role of beta-amyloid (Aβ) co-pathology in PD-MCI variability and progression remains unclear.
Purpose of the Study:
- To investigate how Aβ presence influences clinical and cognitive profiles in PD-MCI.
- To assess the impact of Aβ on regional brain volumes in PD-MCI patients.
Main Methods:
- Simultaneous PET/3T-MRI with [18F]flutemetamol in 25 PD-MCI patients.
- Clinical and neuropsychological assessments for diagnosis.
- Analysis of [18F]flutemetamol standardized uptake value ratios (SUVR) and brain volumes via MRI.
Main Results:
- 8 Aβ+ and 17 Aβ- PD-MCI patients were identified; no significant differences in age, disease duration, or global cognition.
- Aβ+ PD-MCI patients exhibited worse executive function performance (p=0.037).
- Significant Aβ deposition observed in specific cortical and subcortical regions, correlating with executive function deficits.
Conclusions:
- Cerebral Aβ exacerbates executive dysfunction in PD-MCI but does not affect motor or global cognitive abilities.
- Aβ presence is not linked to middle-temporal cortex atrophy in PD-MCI.
- Findings suggest Aβ aggravates deficits related to primary Parkinson's pathology rather than being the main driver of cognitive decline in PD-MCI.
