ArticleJournal of Alzheimer's disease : JAD2022
Characterizing Network Selectiveness to the Dynamic Spreading of Neuropathological Events in Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Pathology steered stratification network for subtype identification in Alzheimer's disease.Medical physics · 2024Article
- Hub overload and failure as a final common pathway in neurological brain network disorders.Network neuroscience (Cambridge, Mass.) · 2024Review
- Learning pyramidal multi-scale harmonic wavelets for identifying the neuropathology propagation patterns of Alzheimer's disease.Medical image analysis · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMounting evidence shows that the neuropathological burdens manifest preference in affecting brain regions during the dynamic progression of Alzheimer's disease (AD). Since the distinct brain regions are physically wired by white matter fibers, it is reasonable to hypothesize the differential spreading pattern of neuropathological burdens may underlie the wiring topology, which can be characterized using neuroimaging and network science technologies.
objectiveTo study the dynamic spreading patterns of neuropathological events in AD.
methodsWe first examine whether hub nodes with high connectivity in the brain network (assemble of white matter wirings) are susceptible to a higher level of pathological burdens than other regions that are less involved in the process of information exchange in the network. Moreover, we propose a novel linear mixed-effect model to characterize the multi-factorial spreading process of neuropathological burdens from hub nodes to non-hub nodes, where age, sex, and APOE4 indicators are considered as confounders. We apply our statistical model to the longitudinal neuroimaging data of amyloid-PET and tau-PET, respectively.
resultsOur meta-data analysis results show that 1) AD differentially affects hub nodes with a significantly higher level of pathology, and 2) the longitudinal increase of neuropathological burdens on non-hub nodes is strongly correlated with the connectome distance to hub nodes rather than the spatial proximity.
conclusionThe spreading pathway of AD neuropathological burdens might start from hub regions and propagate through the white matter fibers in a prion-like manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.