Cognitive reserve and network efficiency in Alzheimer’s disease.
Summary
Background: Cognitive reserve (CR) refers to the ability to compensate for a certain amount of brain damage and sustain cognitive functions. The extent to which Alzheimer’s disease (AD) leads to cognitive decline is believed to be related to the concept of CR. It was expected that an efficiently organized network structure is part of the neural basis of reserve, altering the effects of AD pathology on cognition. The purpose of this study was to explore this hypothesis by investigating the relationship between CR, network connectivity, cognitive functioning, and brain atrophy.
Methods: Fifty patients, with either an AD or Mild Cognitive Impairment (MCI) diagnosis, were included in this study. Memory performance, information processing speed, and executive functioning were assessed by standardized neuropsychological testing. CR was operationalized as the combination of education level and occupational attainment. Brain volumes were assessed and processed diffusion tensor imaging (DTI) data was obtained and used to investigate properties of the structural network that represent network efficiency. Correlation analyses were performed, while controlling for the effects of age.
Results: The results showed higher levels of CR were significantly correlated to longer path length (rs=.155, p=.007) and low smallworldness (rs=-.135, p=.02). Also, a relationship between total brain atrophy and clustering coefficient (rs=-.188, p=.044) and path length (rs =-.201, p=.001) was revealed. Furthermore, a significant correlation between CR and memory performance was found (rs=.359, p=.013): memory performance was better in patients with higher CR. Network efficiency was not directly related to cognitive performance.
Conclusion: Results suggest that network efficiency is more deteriorated in high CR individuals compared to low CR patients, when clinical presentation of AD emerges. Despite the worse network structure, memory performance is still better in patients with higher CR. This might either be due to higher premorbid memory functioning or it could mean memory performance declines at a slower rate as the result of higher CR. Furthermore, network organization was expected to be a neural component of CR leading to better cognitive performance. This might be the case in healthy adults. However, in AD and MCI patients this relationship is greatly affected by the degree of brain damage, as significant correlations were revealed between network efficiency and brain atrophy.