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Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
Published on: August 7, 2017
Caudal and Thalamic Segregation in White Matter Brain Network Communities in Alzheimer's Disease Population
Frederick Xu1, Duy Duong-Tran2, Yize Zhao3
1Department of Bioengineering, University of Pennsylvania, Philadelphia, PA, USA.
Abstract:
Neuroimaging studies have demonstrated that Alzheimer's disease (AD) is closely related to changes in neuroanatomy in the form of damage to both grey matter and white matter. However, the exact nature of AD's relationship with white matter anatomical deterioration is not fully understood at a systemic level. To investigate this knowledge gap, we constructed structural brain networks from ADNI-GO/2 diffusion tensor imaging (DTI) images with brain regions of interest (ROIs) as nodes and white matter connections as edges weighted by fiber density. The cohort consists of healthy control (HC), mild cognitive impairment (MCI), and clinically diagnosed AD subjects. By optimizing consensus modularity of structural brain networks at a subpopulation level to investigate community structure throughout a range of resolution parameters (γ), we observed a split of the reward-based decision-making module in the AD group at γ = 1.3, thus finding a 7th consensus community in the AD consensus brain network partition that was not present in that of MCI or HC populations. Upon further investigation, we found that thalamic and caudal regions were involved in the increased segregation of AD brain networks. These regions are implicated in regulation of decision-making processes, and their segregation from other decision-making regions is a novel finding in white matter biomarker studies of AD. Our study presents novel evidence that AD may be a disconnection syndrome at the mesoscopic structural level, with potential new avenues of exploration into the role of the thalamus and caudate that may reveal neural correlates of cognitive deficits in clinically diagnosed AD.
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