Andrey V. Kuznetsov

This paper develops a mathematical model linking SAA-HDL binding dynamics to renal amyloidosis progression, showing how inflammation patterns and SAA levels affect disease outcomes.

This paper develops a mathematical model of IAPP aggregation in type 2 diabetes, identifying key parameters influencing cytotoxicity and suggesting therapeutic targets.

This study uses a mathematical model to show that TTR aggregation primarily occurs in cardiac tissue, not blood plasma, and predicts fibril accumulation linked to disease progression and mortality.

This paper develops a model linking accumulated neurotoxicity from amyloid beta oligomers to biological age, showing that increasing half-lives of Aβ monomers and oligomers accelerates aging.

The paper shows that hydrodynamic dispersion in porous media enhances viral-cellular collisions, improving transduction efficiency by overcoming sedimentation-diffusion limitations.

This paper develops a mathematical model to simulate Aβ dynamics and quantify accumulated neurotoxicity as a marker of biological age, showing its non-linear relationship with plaque burden and the impact of degradation efficiency.

This study develops a mathematical model to simulate LC aggregation and cardiac injury in AL amyloidosis, showing that cardiac tissue aggregation leads to greater fibril deposition and cardiotoxicity than plasma aggregation.

The paper introduces a metric for measuring accumulated neurotoxicity of alpha-synuclein oligomers and finds that rapid fibril formation reduces toxicity, while impaired degradation increases it.

The paper develops a criterion to quantify accumulated neurotoxicity of Aβ oligomers in Alzheimer's disease, revealing a quadratic relationship between neurotoxicity and time.

This study uses computational simulations to examine ATP transport in axons, showing that spontaneous neuronal firing stabilizes ATP levels and that a single mitochondrion can supply ATP to neighboring boutons, but ATP concentration declines with more empty boutons.

The paper proposes a mathematical model to quantify the combined neurotoxicity of amyloid beta and tau oligomers in Alzheimer's disease and shows how their deposition into plaques and tangles affects toxicity accumulation.

This paper develops a mathematical model to simulate TAF15 inclusion growth in neurons, showing that inclusion growth is maximized at an intermediate deposition rate of free TAF15 aggregates.

This paper models ATP concentration dynamics in presynaptic boutons with and without stationary mitochondria, finding that ATP levels remain sufficient for synaptic activity even without mitochondria.

This study models the growth of senile plaques in Alzheimer's disease, finding that plaque growth depends on the balance between Aβ aggregate deposition and autocatalytic production.