Spatial-temporal interactions between white matter hyperintensities and multiple pathologies across the Alzheimer's
Li Liang1,2, Wei Liu1, Youping Zhong1
1Department of Electronic & Information Engineering, Harbin Institute of Technology (Shenzhen), Shenzhen, China.
Alzheimer's disease (AD) research reveals amyloid beta (Aβ) accumulation drives white matter hyperintensities (WMHs) in specific brain networks. WMHs also correlate with microstructural damage in key white matter tracts.
Area of Science:
- Neuroimaging
- Neuropathology
- Network Neuroscience
Background:
- Alzheimer's disease (AD) and white matter hyperintensities (WMHs) interactions in brain networks are not fully understood.
- Clarifying these relationships is crucial for understanding AD progression.
Purpose of the Study:
- To investigate the dynamic, multiscale interactions between AD pathologies and WMHs.
- To model the interplay of amyloid beta (Aβ), WMHs, and white matter microstructural changes.
Main Methods:
- Utilized data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database.
- Modeled regional WMHs, Aβ accumulation, and microstructural changes using time-evolving graphs.
- Applied Granger causality analysis on pseudo-time subject sequences to determine causal relationships.
Main Results:
- Aβ accumulation was identified as a Granger cause of WMHs in the inferior longitudinal fasciculus (ILF) structural network in 86% of sequences.
- WMHs significantly correlated with microstructural changes (reduced fractional anisotropy) in the ILF, inferior fronto-occipital fasciculus, and cingulum.
Conclusions:
- Findings illuminate the complex, time-dependent interactions between WMHs and AD pathologies.
- Provides insights into the relationship between cerebral small vessel disease and AD.
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