Our last preprint "High-fidelity and network-based spatio-temporal mathematical models of Alzheimer's disease progression and their validation against PET-SUVR imaging data" from B. Caon, F. Bonizzoni, P.F. Antonietti, and me is now out on ArXiv and MOX Report. 

Mathematical models provide a valuable quantitative tool for monitoring Alzheimer's disease progression. In this work, we proposed and compare a novel framework where the spatio-temporal dynamics of amyloid-beta and tau proteins is modeled based on employing either three-dimensional patient-specific geometries or through reduced network-based models defined on the brain connectome. A sensitivity analysis is presented to quantify the influence of model parameters on protein concentration patterns as well as compare the quality of the predictions. For both approaches, the results are validated against PET-SUVR clinical data using 18FAZD4694 for amyloid-beta and 18FMK6240 for tau protein.

I am delighted to announce that I have been awarded, ex aequo, the 2026 GBMA Award for Best PhD Thesis in Theoretical and Applied Biomechanics. The award was presented on April 13, 2026, during the  GBMA–GMA Best PhD Thesis Competition.

The prize is conferred by the Biomechanics Group (GBMA) of the Italian Association of Theoretical and Applied Mechanics (AIMETA). The evaluation committee selected my thesis "Mathematical Models and Numerical Methods for Neurodegenerative Diseases" for its originality and innovative contribution to the development of computational methodologies for modeling complex biological systems.

As part of the award, I will be invited to present my scientific results in a plenary session at the upcoming AIMETA Conference. 

Our last preprint "A whole-brain model of amyloid beta accumulation and cerebral hypoperfusion in Alzheimer's disease" from A. Ahern, A. Goriely, E. Kuhl, P.F. Antonietti, and me is now out on ArXiv and MOX Report. 

Evidence suggests that amyloid beta and cerebrovascular pathology are mutually reinforcing; in particular, amyloid beta suppresses perfusion by constricting capillaries, and hypoperfusion promotes the production of amyloid beta. Here, we propose a whole-brain model coupling amyloid beta and blood vessel through a hybrid model consisting of a reaction-diffusion system for the protein dynamics and porous-medium model of blood flow within and between vascular networks. Simulations in realistic brain geometries demonstrate the emergence of multistability, implying that a sufficiently large pathogenic protein seeds is necessary to trigger disease outbreak. Motivated by the "two-hit vascular hypothesis" of Alzheimer's disease that hypoperfusive vascular damage triggers amyloid beta pathology, we also demonstrate that localized hypoperfusion, in response to injury, can destabilize the healthy steady state and trigger brain-wide disease outbreak. 

Polygonal and Structure-Preserving Methods for PDEs Discretization

Mathematical Modeling of Neurodegenerative Diseases