ArticleProceedings. Mathematical, physical, and engineering sciences2018
Simulating the effect of formation of amyloid plaques on aggregation of tau protein.
Article in Proceedings. Mathematical, physical, and engineering sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 31 citations in OpenAlex.
- A network-level transport model of tau progression in the Alzheimer's brain.Mathematical medicine and biology : a journal of the IMA · 2025Article
- Personalized Computational Causal Modeling of the Alzheimer Disease Biomarker Cascade.The journal of prevention of Alzheimer's disease · 2024Article
- A scoping review of mathematical models covering Alzheimer's disease progression.Frontiers in neuroinformatics · 2024Article
- Dynein Dysfunction Prevents Maintenance of High Concentrations of Slow Axonal Transport Cargos at the Axon Terminal: A Computational Study.Journal of biomechanical engineering · 2023Article
- Deep learning application for the classification of Alzheimer's disease usingScientific reports · 2023Article
- Machine learning application for classification of Alzheimer's disease stages usingBiomedical engineering online · 2023Article
- Connectome-based biophysics models of Alzheimer's disease diagnosis and prognosis.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Emergence of directional bias in tau deposition from axonal transport dynamics.PLoS computational biology · 2021Article
- Modeling tau transport in the axon initial segment.Mathematical biosciences · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this paper, we develop a mathematical model that enables the investigation of the production and intracellular transport of amyloid precursor protein (APP) and tau protein in a neuron. We also investigate the aggregation of APP fragments into amyloid-β (Aβ) as well as tau aggregation into tau oligomers and neurofibrillary tangles. Using the developed model, we investigate how Aβ aggregation can influence tau transport and aggregation in both the soma and the axon. We couple the Aβ and tau agglomeration processes by assuming that the value of the kinetic constant that describes the autocatalytic growth (self-replication) reaction step of tau aggregation is proportional to the Aβ concentration. The model predicts that APP and tau are distributed differently in the axon. While APP has a uniform distribution along the axon, tau's concentration first decreases and then increases towards the synapse. Aβ is uniformly produced along the axon while misfolded tau protein is mostly produced in the proximal axon. The number of Aβ and tau polymers originating from the axon is much smaller than the number of Aβ and tau polymers originating from the soma. The rate of production of misfolded tau polymers depends on how strongly their production is facilitated by Aβ.
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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.