Alzheimer’s disease has a long preclinical phase during which amyloid pathology and neurodegeneration accumulate in the brain without producing cognitive deficits. It is currently unclear whether these early disease stages are associated with a progressive disruption in the communication between brain regions that might lead to clinical decline and dementia.
In this study we assessed the organization of the structural networks in cognitively normal (CN) individuals harbouring amyloid pathology (A+N-), neurodegeneration (A-N+) or both (A+N+). We combined graph theory with diffusion tensor imaging to investigate integration, segregation and centrality measures in the brain connectome of the previous groups.
At baseline, our findings revealed a disrupted network topology characterized by larger paths, lower efficiency, increased clustering and modularity in CN A-N+ and CN A+N+. After two years, CN A+N+ showed a progressive increase in the clustering, whereas no changes were observed in the other groups. Network topology correlated with cognitive speed in all groups and with memory performance specifically in CN A+N+.
Altogether, our findings suggest that amyloid pathology is not sufficient to disrupt structural network topology, whereas neurodegeneration is. In contrast to CN A-N+, network organization in CN A+N+ individuals continued to decline over time and was associated with memory functions.
© 2017 Published by Elsevier Inc.