Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the deposition, over decades, of pathogenic forms of two proteins, amyloid-beta and misfolded tau. The study focuses on the misfolded forms of tau within neurons and considers the so called prionic hypothesis: a pathological tau molecule may induce its misfolding in a healthy tau protein. The transmission of the misfolded tau molecules through synapses is also considered. Thus, an epidemic model that considers epidemic transmission among 5 areas in the brain (for a single hemisphere) is set up: Entorhinal Cortex (EC), Hyppocampus, Inferior Temporal Gyrus, Middle Frontal Gyrus and Calcarine Cortex. The model uses both available experimental neurochemical information, that quantifies excitation and inhibition, and neuroimaging data as a proxy of inter-region connectivity. The model is very predictive in determining the main experimentally available information, that is the sequence in which the disease appears starting from the known area where it originates (EC).
Supervisors: José Javier Ramasco, Manuel A. Matias, and Alfredo Ramos Miguel
Jury members: Claudio Mirasso, Sandro Meloni, and Manuel A. Matias
The defense will be presential and will be broadcasted through Zoom:
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