Abstract
Brain connectivity analysis has shown great promise in understanding how aging affects functional connectivity; however, an explanatory framework to study healthy aging in terms of network efficiency is still missing. Here, we study network robustness, i.e., resilience to perturbations, in resting-state functional connectivity networks (rs-fMRI) in young and elder subjects. We apply analytic measures of network communication efficiency in the human brain to investigate the compensatory mechanisms elicited in aging. Specifically, we quantify the effect of “lesioning” (node canceling) of either single regions of interest (ROI) or whole networks on global connectivity metrics (i.e., efficiency). We find that young individuals are more resilient than old ones to random “lesioning” of brain areas; global network efficiency is over 3 times lower in older subjects relative to younger subjects. On the other hand, the “lesioning” of central and limbic structures in young subjects yield a larger efficiency loss than in older individuals. Overall, our study shows a more idiosyncratic response to specific brain network “lesioning” in elder compared to young subjects, and that young adults are more resilient to random deletion of single nodes compared to old adults.
Highlights
The concept of brain reserve has its origins in the experimental observation of the mismatch between disease-related changes in the brain and the clinical manifestation of those changes
We explore the hypothesis that normal aging is associated with changes in network efficiency
The imaging area consisted of 32 functional gradient-echo planar imaging (EPI) axial slices that were used to obtain T2*-weighted fMRI images in the axial plane
Summary
The concept of brain reserve has its origins in the experimental observation of the mismatch between disease-related changes in the brain and the clinical manifestation of those changes. Postmortem analysis of people with Alzheimer’s disease showed a non-negligible number of individuals with fewer clinical symptoms than the pathological features suggested (Katzman et al, 1988). These individuals have heavier brains containing more neurons or a greater “reserve” that could help fight cognitive decline associated with brain damage, e.g., neuronal loss (Crystal et al, 1988; Guo et al, 2013). The concept of reserve or resilience can help to explain the neuroprotective effects triggered by brain changes and is supported by structural
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