Category: Parkinson's Disease: Neuroimaging
Objective: To investigate the potential association between cerebral amyloid (Aβ) deposition and regional brain metabolism in patients with Parkinson’s disease (PD)
Background: Although Parkinson’s disease (PD) is primarily characterized by intraneuronal α-synucleinopathy, emerging evidence suggests that it often coexists with other pathological features, particularly amyloid pathology. The presence of concomitant amyloid pathology in Parkinson’s disease has been associated with a poorer prognosis, characterized by accelerated cognitive decline and reduced survival. Nevertheless, there is scant evidence elucidating the influence of amyloid pathology on cerebral glucose metabolism in patients with PD.
Method: In this retrospective cross-sectional observational study, we included 39 patients with PD (dementia, n = 24; non-demented, n = 15) and 25 healthy controls who underwent both 18F-Fluorodeoxyglucose (18F-FDG) and 18F-Florbetaben (18F-FBB) positron emission topography (PET). Regional 18F-FDG uptake were compared across amyloid-positive (Aβ+) PD, amyloid-negative (Aβ-) PD, and Aβ- CU subjects. Furthermore, partial correlation analyses were employed to investigate the association between regional 18F-FDG uptake and global and regional 18F-FBB uptake within PD patients using age, sex, education years, and disease duration as covariates.
Results: Compared to healthy controls, PD patients revealed hypometabolism in the prefrontal, temporal, parieto-occipital regions regardless of amyloid status. Within patients with PD, Aβ+ group exhibited more severe glucose hypometabolism in anterior cingulate cortex, caudate, amygdala, and nucleus accumbens compared to Aβ- PD group. While global 18F-FBB uptake showed significant negative correlation with 18F-FDG uptake amygdala (rho = -0.492, P = 0.003), caudate (rho = -0.350, 0.043), insular (rho = -0.357, P = 0.038) and anterior cingulate cortex (rho = -0.360, P = 0.037) in a dose-dependent manner, significant intra-regional relationships between 18F-FBB and 18F-FDG was observed in the anterior cingulate cortex only (rho = -0.330, P = 0.049).
Conclusion: Our findings suggest that cerebral amyloidosis may contribute to altered patterns of the regional cerebral glucose metabolism in patients with PD.
To cite this abstract in AMA style:
HK. Na, Y. Sun, JH. Lee, CW. Park, YH. Sohn, CH. Lyoo, PH. Lee. Association Between Cerebral Glucose Metabolism and Amyloid Deposition in Parkinson’s Disease [abstract]. Mov Disord. 2024; 39 (suppl 1). https://www.mdsabstracts.org/abstract/association-between-cerebral-glucose-metabolism-and-amyloid-deposition-in-parkinsons-disease/. Accessed May 17, 2025.« Back to 2024 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/association-between-cerebral-glucose-metabolism-and-amyloid-deposition-in-parkinsons-disease/