ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Spatial-temporal interactions between white matter hyperintensities and multiple pathologies across the Alzheimer's disease continuum.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Contributions of the Alzheimer's Disease Neuroimaging Initiative to advancing AD research: a targeted review of recent publications.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Cerebral Small Vessel Disease as a Novel Risk Indicator for Periodontitis Progression.International dental journal · 2026Article
- Spatial-temporal interactions between white matter hyperintensities and multiple pathologies across the Alzheimer's disease continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Polygenic risk for white matter hyperintensities is associated with early cerebrovascular events partly through hemodynamic measures in cognitively unimpaired middle-aged and older adults with low cardiovascular risk.Frontiers in neurology · 2025Article
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Authors and funding
6 authors.
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Abstract
introductionThe interactive relationships between Alzheimer's disease (AD) and white matter hyperintensities (WMHs) in multiscale brain structural networks still need to be clarified.
methodsBased on subjects enrolled from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, regional WMHs, amyloid beta (Aβ) accumulation, and microstructural changes detected by diffusion weighted imaging (DWI) in multiscale brain networks were modeled by time-evolving graphs; their interactive relationships were further investigated using Granger causality after constructing pseudo-time subject sequences.
resultsIn up to 86% of the extracted pseudo-time subject sequences, Aβ was determined to be the Granger cause of WMHs in the structural connectivity of the inferior longitudinal fasciculus (ILF). Meanwhile WMHs were significantly correlated with microstructural changes measured by reduced fractional anisotropy in the inferior fronto-occipital fasciculus, ILF, and cingulum, which Granger causality pathways detected in 91%, 94%, and 93% of pseudo-time subject sequences, respectively. DISCUSSION: These findings provide novel insights for understanding the multiscale space-time interactions between WMHs and AD pathologies. HIGHLIGHTS: This study proposed time-evolving graph modeling of heterogeneous disease markers (amyloid beta [Aβ], white matter hyperintensities [WMHs], and microstructural changes of white matter tracts) across the Alzheimer's disease (AD) continuum to investigate their complex interactions in multiscale brain structural networks. Regional accumulation of Aβ promoted WMH progression in subnetworks connected by the inferior longitudinal fasciculus (ILF). Regional WMHs were strongly associated with bundle-specific microstructural changes in the ILF, inferior fronto-occipital fasciculus, and cingulum. These results might provide novel insights for understanding the interactive relationship between cerebral small vessel disease and AD.
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