Abstract
Cognitive reserve is the ability to sustain cognitive function even with a certain amount of brain damages. Here we investigate the neural compensation mechanism of cognitive reserve from the perspective of structural brain connectivity. Our goal was to show that normal people with high education levels (i.e., cognitive reserve) maintain abundant pathways connecting any two brain regions, providing better compensation or resilience after brain damage. Accordingly, patients with high education levels show more deterioration in structural brain connectivity than those with low education levels before symptoms of Alzheimer’s disease (AD) become apparent. To test this hypothesis, we use network flow measuring the number of alternative paths between two brain regions in the brain network. The experimental results show that for normal aging, education strengthens network reliability, as measured through flow values, in a subnetwork centered at the supramarginal gyrus. For AD, a subnetwork centered at the left middle frontal gyrus shows a negative correlation between flow and education, which implies more collapse in structural brain connectivity for highly educated patients. We conclude that cognitive reserve may come from the ability of network reorganization to secure the information flow within the brain network, therefore making it more resistant to disease progress.
Highlights
Cognitive reserve is the ability to sustain cognitive function even with a certain amount of brain damages
The results support the existence of hypothesized neural mechanisms for cognitive reserve based on network flow analysis of binary white matter (WM) brain networks
We identified two subnetworks of the WM brain networks that might represent cognitive reserve
Summary
Cognitive reserve is the ability to sustain cognitive function even with a certain amount of brain damages. The Nun Study showed that more highly educated nuns had fewer symptoms of cognitive decline[3] These observations imply that normal people with the same cognitive function may have different levels of brain pathology according to the amount of their cognitive reserve. A study using positron emission tomography (PET) demonstrated that the early-onset AD patients with presumably higher cognitive reserve had more hypometabolic areas than the late-onset AD patients with similar clinical severity[13] These studies speculated on the existence of cognitive reserve by showing lower resting rCBF or higher task-induced activity in individuals with high reserve, but it is still challenging to provide direct and quantitative neural measures of cognitive reserve[4]
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