arXiv subjects

Veronica Tora

Publications and source records attributed to Veronica Tora.

4 recordsLinked to original sources

arXiv2026

The Critical Patch Size Problem in Random Graphs

The problem of {\it critical patch size} -- a threshold condition for population persistence -- is investigated in the context of discrete habitats, modeled as graphs with a distinguished subset of vertices acting as sinks. These sinks impose boundary-like constraints analogous to Dirichlet conditions in continuous domains. The population proliferates locally at the vertices and diffuse across the network through the graph Laplacian. In the sinks the population cannot survive. The Dirichlet eigenvalue of the habitat is defined as the smallest eigenvalue of the principal submatrix of the Laplacian obtained by removing the rows and columns associated with sink vertices. This spectral parameter governs the habitat's viability: survival occurs when the Dirichlet eigenvalue of the habitat lies below a critical reaction-to-diffusion ratio. We study survival conditions for a sequence of random habitats built on binomial random graphs. We establish a law of large numbers for the corresponding sequence of Dirichlet eigenvalues and prove the emergence of a sharp threshold phenomenon: with high probability, a large random habitat is either viable or non-viable, depending on whether the reaction-to-diffusion ratio lies below or above this threshold. Our results provide the first general spectral theory for critical patch size on graphs, with implications for ecology, synthetic biology, and the modeling of processes on brain connectomes.

math.PR↗

arXiv2024

A network-level transport model of tau progression in the Alzheimer's brain

One of the hallmarks of Alzheimer's disease (AD) is the accumulation and spread of toxic aggregates of tau protein. The progression of AD tau pathology is thought to be highly stereotyped, which is in part due to the fact that tau can spread between regions via the white matter tracts that connect them. Mathematically, this phenomenon has been described using models of "network diffusion", where the rate of spread of tau between brain regions is proportional to its concentration gradient and the amount of white matter between them. Although these models can robustly predict the progression of pathology in a wide variety of neurodegenerative diseases, including AD, an under explored aspect of tau spreading is that it is governed not simply by diffusion but also active transport along axonal microtubules. Spread can therefore take on a directional bias, resulting in distinct patterns of deposition, but current models struggle to capture this phenomenon. Recently, we have developed a mathematical model of the axonal transport of toxic tau proteins that takes into account the effects tau exerts on the molecular motors. Here we describe and implement a macroscopic version of this model, which we call the Network Transport Model (NTM). A key feature of this model is that, while it predicts tau dynamics at a regional level, it is parameterized in terms of only microscopic processes such as aggregation and transport rates; that is, differences in brain-wide tau progression can be explained by its microscopic properties. We provide numerical evidence that, as with the two-neuron model that the NTM extends, there are distinct and rich dynamics with respect to the overall rate of spread and the staging of pathology when we simulated the NTM on the hippocampal subnetwork. The theoretical insights provided by the NTM have broad implications for understanding AD pathophysiology more generally.

math.AP↗

arXiv2022

The role of beta-amyloid and tau proteins in Alzheimer's disease: a mathematical model on graph

In this Note we study a mathematical model for the progression of Alzheimer's Disease in the human brain. The novelty of our approach consists in the representation of the brain as two superposed graphs where toxic proteins diffuse, the connectivity graph which represents the neural network, and the proximity graph which takes into account the extracellular space. Toxic proteins such as beta-amyloid and tau play in fact a crucial role in the development of Alzheimer's disease and, separately, have been targets of medical treatments. Recent biomedical literature stresses the potential impact of the synergetic action of these proteins. We numerically test various modelling hypotheses which confirm the relevance of this synergy.

math.AP↗

arXiv2022

Two kinetic models for non-instantaneous binary alignment collisions

A new type of kinetic models with non-instantaneous binary collisions is considered. Collisions are described by a transport process in the joint state space of a pair of particles. The interactions are of alignment type, where the states of the particles approach each other. For two spatially homogeneous models with deterministic or stochastic collision times existence and uniqueness of solutions, the long time behavior, and the instantaneous limit are considered, where the latter leads to standard kinetic models of Boltzmann type.

math.AP↗