The misconformation and aggregation of the protein Amyloid-Beta (A[Formula: see text]) is a key event in the propagation of Alzheimer's Disease (AD). Different types of assemblies are identified, with long fibrils and plaques deposing during the late stages of AD. In the earlier stages, the disease spread is driven by the formation and the spatial propagation of small amorphous assemblies called oligomers. We propose a model dedicated to studying those early stages, in the vicinity of a few neurons and after a polymer seed has been formed. We build a reaction-diffusion model, with a Becker-Döring-like system that includes fragmentation and size-dependent diffusion. We hereby establish the theoretical framework necessary for the proper use of this model, by proving the existence of solutions using a fixed point method.
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Med Image Anal
January 2025
School of Biomedical Engineering and Imaging Sciences, King's College London, UK. Electronic address:
Atrial fibrillation (AF), impacting nearly 50 million individuals globally, is a major contributor to ischaemic strokes, predominantly originating from the left atrial appendage (LAA). Current clinical scores like CHA₂DS₂-VASc, while useful, provide limited insight into the pro-thrombotic mechanisms of Virchow's triad-blood stasis, endothelial damage, and hypercoagulability. This study leverages biophysical computational modelling to deepen our understanding of thrombogenesis in AF patients.
View Article and Find Full Text PDFJ Math Biol
January 2025
Department of Integrative Biology, Oklahoma State University, Stillwater, OK, 74078, USA.
In the past several decades, much attention has been focused on the effects of dispersal on total populations of species. In Zhang (EL 20:1118-1128, 2017), a rigorous biological experiment was performed to confirm the mathematical conclusion: Dispersal tends to enhance populations under a suitable hypothesis. In addition, mathematical models keeping track of resource dynamics in population growth were also proposed in Zhang (EL 20:1118-1128, 2017) to understand this remarkable phenomenon.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Life Sciences, Imperial College, London, SW7 2AZ, UK.
Many cellular patterns exhibit a reaction-diffusion component, suggesting that Turing instability may contribute to pattern formation. However, biological gene-regulatory pathways are more complex than simple Turing activator-inhibitor models and generally do not require fine-tuning of parameters as dictated by the Turing conditions. To address these issues, we employ random matrix theory to analyze the Jacobian matrices of larger networks with robust statistical properties.
View Article and Find Full Text PDFbioRxiv
January 2025
Department of Ecology and Evolutionary Biology, University of Connecticut, Storrs, CT 06269, USA.
The reaction-diffusion (RD) system is widely assumed to account for many complex, self-organized pigmentation patterns in natural organisms. However, the specific configurations of such RD networks and how RD systems interact with positional information (i.e.
View Article and Find Full Text PDFPLoS One
January 2025
School of Chemical Engineering, National Technical University of Athens, Zografou, Athens, Greece.
The aim of this study is to demonstrate the enhanced efficiency of combined therapeutic strategies for the treatment of growing tumors, based on computational experiments of a continuous-level modeling framework. In particular, the tumor growth is simulated within a host tissue and treated as a multiphase fluid, with each cellular species considered as a distinct fluid phase. Our model integrates the impact of chemical species on tumor dynamics, and we model -through reaction-diffusion equations- the spatio-temporal evolution of oxygen, vascular endothelial growth factor (VEGF) and chemotherapeutic agents.
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