Abstract
Magnetic resonance imaging (MRI) offers significant insight into the complex organization of neural networks within the human brain. Using resting-state functional MRI data, topological maps can be created to visualize changes in brain activity, as well as to represent and assess the structural and functional connections between different brain regions. Crucially, Alzheimer’s disease (AD) is associated with progressive loss in this connectivity, which is particularly evident within the default mode network. In this paper, we review the recent literature on how factors that are associated with risk of dementia may influence the organization of the brain network structures. In particular, we focus on cognitive reserve and the common genetic polymorphisms of APOE and BDNF Val66Met.
Highlights
It was estimated that more than 47 million elderly people are affected by dementia globally (Alzheimer’s Disease International, 2009; Prince et al, 2016) and that an additional 131 million people will develop this health-challenging syndrome by 2050 (Prince et al, 2016)
Studies investigating the association of education and cognitive decline in Alzheimer’s disease (AD) have found that more highly educated individuals are able to tolerate more neuropathology before the clinical expression of AD (Bennett et al, 2003), potentially because education moderates the relationship between brain pathological load and cognitive impairments (Brayne et al, 2010; Valenzuela et al, 2011), as well as functional connections (Marques et al, 2016)
Studies reported that Apolipoprotein E (APOE) ε4 was associated with decreased functional connectivity (Lu et al, 2017) and longer path length in functional networks (Goryawala et al, 2015)
Summary
It was estimated that more than 47 million elderly people are affected by dementia globally (Alzheimer’s Disease International, 2009; Prince et al, 2016) and that an additional 131 million people will develop this health-challenging syndrome by 2050 (Prince et al, 2016). Entorhinal-hippocampal circuits are compromised early in AD, followed by the gradual disconnection of the MTL, and the loss of connectivity between association neocortices (Morrison and Hof, 1997) This pattern of progressive and degenerative pathology may underlie the deterioration of certain cognitive functions during aging, leading eventually to frank AD. This review focuses on the methods with which brain connectivity is analyzed, the changes in structural and functional networks found in AD, and the role of cognitive reserve and specific genetic factors in partially determining functional brain connectivity In this regard, potential changes in functional connectivity and resistance to pathology will involve both non-modifiable and modifiable factors that will impact on how brain systems respond to accumulating pathological burden. We discuss features of structural and functional brain networks in relation to genetic biomarkers and environmental factors linked to AD risk, progression and resilience
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