Fig. 1: Schematic AD personalized pathophysiological whole-brain models. | Communications Biology

Fig. 1: Schematic AD personalized pathophysiological whole-brain models.

From: Personalized whole-brain neural mass models reveal combined Aβ and tau hyperexcitable influences in Alzheimer’s disease

Fig. 1

a Individuals underwent a multimodal assessment including structural and resting-state functional MRI, Aβ and tau-PET, clinically relevant plasma biomarkers, and cognitive evaluations. b In the Alzheimer’s disease model, the subject’s neuronal excitability profile is defined as a function of Aβ, tau and the synergistic interaction of Aβ and tau. Regional excitatory and inhibitory firing rates are influenced by the local pathophysiological profiles and the signals coming from other regions via an average anatomical connectome. The regional neuronal signals generate BOLD indicators through metabolic/hemodynamic transformations. By maximizing the similarity between the generated and observed BOLD data, the set of subject-specific influences of the pathophysiological Aβ, tau and Aβ·tau factors on neuronal activity are quantified. c These estimated pathophysiological influences serve to recover electrophysiological activity producing the real individual BOLD signals, and to study individual excitability profiles and their relationship with independent AD (plasma) markers and cognitive deterioration. Volumetric brain views in the figure were generated with SurfStat (https://www.math.mcgill.ca/keith/surfstat/).

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