Fig. 2

AD-mediated microscale neuronal hyperactivity and its translation to large-scale EEG/MEG signals. A By using a computational brain network model, we can implement empirically informed AD neuronal pathology as measured by single cell patch-clamp recordings, microcircuit local field potentials, or calcium imaging, and investigate the effects on macroscale brain oscillations as measured by whole-brain EEG/MEG in human prodromal AD patients. B Schematic illustration of the different scenarios of AD-mediated changes in neuronal activity implemented in the model. Scenario 1: pyramidal neuronal hyperactivity by simulation of A: (intrinsically) increased excitability of excitatory neurons, or by B: increased excitatory postsynaptic potentials of pyramidal (and inhibitory) neurons, or by C: increased excitatory to excitatory coupling strength. Scenario 2: inhibitory neuronal dysfunction by simulation of A: (intrinsically) decreased excitability of inhibitory neurons, or by B: decreased inhibitory postsynaptic potential in the excitatory population, or by C: decreased inhibitory to excitatory synaptic coupling. C Simplified presentation of the computational dynamic brain network model used in this study. Only two coupled neural masses are shown for simplicity. The number-letter combinations correspond to the different AD-like scenarios in B and their location reflects the virtual spatial location. For more details about the scenarios, we refer to Table 2