ArticlePLoS computational biology2014
Epidemic spreading model to characterize misfolded proteins propagation in aging and associated neurodegenerative disorders.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
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- In silico models in oncology, neurology, and epidemiology: systems-level and multiscale perspectives.NPJ systems biology and applications · 2026Review
- Neuronal activity and amyloid-β promote tau seeding in the entorhinal cortex in Alzheimer's disease.Brain : a journal of neurology · 2026Article
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Structure-function coupling in the human brainstem.bioRxiv : the preprint server for biology · 2026Article
- Rise-and-fall dynamics reveal a molecular and cellular vulnerability axis in prion-likebioRxiv : 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
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- A complex network perspective on brain disease.Biological reviews of the Cambridge Philosophical Society · 2026Review
- LNODE: Uncovering the Latent Dynamics ofMedical image computing and computer-assisted intervention : MICCAI ... International Conference on Medical Image Computing and Computer-Assisted Intervention · 2026Article
- Novel applications of machine learning and computational neuroscience models to neuroimaging in Parkinson's disease and related disorders.Frontiers in aging neuroscience · 2026Review
- Structural and functional covariance architecture of major depressive disorder: A meta-analytic structural equation modeling approach to primary neuroimaging analysis.Brain organoid & systems neuroscience journal · 2025Article
- Synaptic loss pattern is constrained by brain connectome and modulated by phosphorylated tau in Alzheimer's disease.Nature communications · 2025Article
- A single-snapshot inverse solver for two-species graph model of tau pathology spreading in human Alzheimer's disease.Brain informatics · 2025Article
- Mapping cerebral blood perfusion and its links to multi-scale brain organization across the human lifespan.PLoS biology · 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
45 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Misfolded proteins (MP) are a key component in aging and associated neurodegenerative disorders. For example, misfolded Amyloid-ß (Aß) and tau proteins are two neuropathogenic hallmarks of Alzheimer's disease. Mechanisms underlying intra-brain MP propagation/deposition remain essentially uncharacterized. Here, is introduced an epidemic spreading model (ESM) for MP dynamics that considers propagation-like interactions between MP agents and the brain's clearance response across the structural connectome. The ESM reproduces advanced Aß deposition patterns in the human brain (explaining 46∼56% of the variance in regional Aß loads, in 733 subjects from the ADNI database). Furthermore, this model strongly supports a) the leading role of Aß clearance deficiency and early Aß onset age during Alzheimer's disease progression, b) that effective anatomical distance from Aß outbreak region explains regional Aß arrival time and Aß deposition likelihood, c) the multi-factorial impact of APOE e4 genotype, gender and educational level on lifetime intra-brain Aß propagation, and d) the modulatory impact of Aß propagation history on tau proteins concentrations, supporting the hypothesis of an interrelated pathway between Aß pathophysiology and tauopathy. To our knowledge, the ESM is the first computational model highlighting the direct link between structural brain networks, production/clearance of pathogenic proteins and associated intercellular transfer mechanisms, individual genetic/demographic properties and clinical states in health and disease. In sum, the proposed ESM constitutes a promising framework to clarify intra-brain region to region transference mechanisms associated with aging and neurodegenerative disorders.
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