ArticleBrain communications2022
Differentiating amyloid beta spread in autosomal dominant and sporadic Alzheimer's disease.
Article in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Highly Efficient and Eco-friendly Synthesis and Bio-activities of 1,3-benzazoles as Cu (II) Chelators in Alzheimer's Disease Therapy.Current medicinal chemistry · 2026Article
- Analyzing heterogeneity in Alzheimer disease using multimodal normative modeling on imaging-based ATN biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Connectome-based biophysical models of pathological protein spreading in neurodegenerative diseases.PLoS computational biology · 2025Review
- Article
- IMPROVING NORMATIVE MODELING FOR MULTI-MODAL NEUROIMAGING DATA USING MIXTURE-OF-PRODUCT-OF-EXPERTS VARIATIONAL AUTOENCODERS.Proceedings. IEEE International Symposium on Biomedical Imaging · 2024Article
- Is Alzheimer disease a disease?Nature reviews. Neurology · 2024Review
- Connectome-based modelling of neurodegenerative diseases: towards precision medicine and mechanistic insight.Nature reviews. Neuroscience · 2023Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Amyloid-beta deposition is one of the hallmark pathologies in both sporadic Alzheimer's disease and autosomal-dominant Alzheimer's disease, the latter of which is caused by mutations in genes involved in amyloid-beta processing. Despite amyloid-beta deposition being a centrepiece to both sporadic Alzheimer's disease and autosomal-dominant Alzheimer's disease, some differences between these Alzheimer's disease subtypes have been observed with respect to the spatial pattern of amyloid-beta. Previous work has shown that the spatial pattern of amyloid-beta in individuals spanning the sporadic Alzheimer's disease spectrum can be reproduced with high accuracy using an epidemic spreading model which simulates the diffusion of amyloid-beta across neuronal connections and is constrained by individual rates of amyloid-beta production and clearance. However, it has not been investigated whether amyloid-beta deposition in the rarer autosomal-dominant Alzheimer's disease can be modelled in the same way, and if so, how congruent the spreading patterns of amyloid-beta across sporadic Alzheimer's disease and autosomal-dominant Alzheimer's disease are. We leverage the epidemic spreading model as a data-driven approach to probe individual-level variation in the spreading patterns of amyloid-beta across three different large-scale imaging datasets (2 sporadic Alzheimer's disease, 1 autosomal-dominant Alzheimer's disease). We applied the epidemic spreading model separately to the Alzheimer's Disease Neuroimaging initiative (
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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.