Network Patterns of Beta-Amyloid Deposition in Parkinson's Disease

Abstract

Beta-amyloid (Aβ) in the brain is a key pathological feature of certain neurodegenerative diseases. Recent studies using graph theory have shown that Aβ brain networks are of pathological significance in Alzheimer's disease (AD). However, the characteristics of Aβ brain networks in Parkinson's disease (PD) are unknown. In the present study using positron emission tomography (PET) with [¹¹C]-Pittsburgh compound B (PiB), we applied a graph theory-based analysis to assess the topological properties of Aβ brain network in PD patients with and without Aβ burden (PiB-positive and PiB-negative, respectively) and healthy controls with Aβ burden. We found that the PD PiB-positive group demonstrated significantly lower value in global efficiency and modularity compared with PD PiB-negative group. The less robust modular structure indicates the tendency of having increased inter-modular connections than intra-modular connectivity (i.e., reduced segregation). Results of hub organization showed that relative to PD PiB-negative group, different hubs were identified in the PiB-positive group, which were located mainly within the default mode network. Overall, our findings suggest disturbances in Aβ topological organization characterized by abnormal network integration and segregation in PD patients with Aβ burden. The stronger inter-modular connectivity observed in the PD PiB-positive group may suggest the spreading pattern of Aβ between modules in those PD patients with elevated PiB burden, thus providing insight into the beta-amyloidopathy of PD.

Keywords: Beta-amyloid; Graph theory; Parkinson’s disease; Pittsburgh compound B positron emission tomography (PiB-PET).