Prior studies have used PET-based amyloid and tau deposition to modulate local excitability and mimic E/I imbalance [29, 61]; likewise, our model can potentially simulate shifts from early-stage hyperexcitability and hyperconnectivity toward later hypoexcitable, spectrally slowed states, reflecting the progression from preclinical to symptomatic stages of dementia [28, 62]. This evidence concerns the gene MAPT and dementia.