ArticleJournal of the Royal Society, Interface2019
Prion-like spreading of Alzheimer's disease within the brain's connectome.
Article in Journal of the Royal Society, Interface, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 143 citations in OpenAlex.
- Alzheimer's Disease Accelerates Cerebral Atrophy by Over a Decade Compared to Healthy Aging.Annals of biomedical engineering · 2026Article
- Global network and local vulnerabilities underlie brain atrophy across Parkinson's disease stages.Brain : a journal of neurology · 2026Article
- Neuronal activity and amyloid-β promote tau seeding in the entorhinal cortex in Alzheimer's disease.Brain : a journal of neurology · 2026Article
- Model Validation Pipeline Against Longitudinal Alzheimer's Biomarker Data.Neuroinformatics · 2026Article
- Theory and simulations of delayed stochastic and deterministic models of prion diseases.Journal of mathematical biology · 2026Article
- A multiscale theory for network advection- reaction-diffusion.Journal of mathematical biology · 2026Article
- Structure-function coupling in the human brainstem.bioRxiv : the preprint server for biology · 2026Article
- Brain network dynamics determine tau presence while regional vulnerability governs tau load in Alzheimer's disease.Research square · 2026Article
- Network Diffusion Modeling in Computational Neuroscience.Advances in experimental medicine and biology · 2026Article
- A computational framework to predict the spreading of Alzheimer's disease.Engineering with computers · 2026Article
- Novel anti-prion compounds screening in prion-infected cell culture model combined with surface plasmon resonance analysis.Scientific reports · 2025Article
- Patient-specific functional brain architecture explains cortical patterns of tau PET in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- A single-snapshot inverse solver for two-species graph model of tau pathology spreading in human Alzheimer's disease.Brain informatics · 2025Article
- Personalised regional modelling predicts tau progression in the human brain.PLoS biology · 2025Article
- Back to the Future: Predicting Individual Tau Progression in Alzheimer's Disease.Research square · 2025Article
- Understanding the complex interplay between tau, amyloid and the network in the spatiotemporal progression of Alzheimer's disease.Progress in neurobiology · 2025Article
- Convergent large-scale network and local vulnerabilities underlie brain atrophy across Parkinson's disease stages: a worldwide ENIGMA study.medRxiv : the preprint server for health sciences · 2025Article
- A network-level transport model of tau progression in the Alzheimer's brain.Mathematical medicine and biology : a journal of the IMA · 2025Article
- Network Diffusion-Constrained Variational Generative Models for Investigating the Molecular Dynamics of Brain Connectomes Under Neurodegeneration.International journal of molecular sciences · 2025Article
- Linking dietary patterns to Alzheimer's disease biomarkers with network mathematical modeling could enable new approach methodologies in preventative AD research: a narrative interdisciplinary review.Frontiers in nutrition · 2025Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prion hypothesis states that misfolded proteins can act as infectious agents that template the misfolding and aggregation of healthy proteins to transmit a disease. Increasing evidence suggests that pathological proteins in neurodegenerative diseases adopt prion-like mechanisms and spread across the brain along anatomically connected networks. Local kinetic models of protein misfolding and global network models of protein spreading provide valuable insight into several aspects of prion-like diseases. Yet, to date, these models have not been combined to simulate how pathological proteins multiply and spread across the human brain. Here, we create an efficient and robust tool to simulate the spreading of misfolded protein using three classes of kinetic models, the Fisher-Kolmogorov model, the Heterodimer model and the Smoluchowski model. We discretize their governing equations using a human brain network model, which we represent as a weighted Laplacian graph generated from 418 brains from the Human Connectome Project. Its nodes represent the anatomic regions of interest and its edges are weighted by the mean fibre number divided by the mean fibre length between any two regions. We demonstrate that our brain network model can predict the histopathological patterns of Alzheimer's disease and capture the key characteristic features of finite-element brain models at a fraction of their computational cost: simulating the spatio-temporal evolution of aggregate size distributions across the human brain throughout a period of 40 years takes less than 7 s on a standard laptop computer. Our model has the potential to predict biomarker curves, aggregate size distributions, infection times, and the effects of therapeutic strategies including reduced production and increased clearance of misfolded protein.
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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.