Of numerous mouse models of Alzheimer’s disease we chose to study the humanized knock-in second generation mouse model of AD (Saito, T, 2014). thought to be superior to overexpressing transgenic mouse models (Sasaguri, H, 2017). Our working hypothesis is that heightened network excitability is present during the early stages of Alzheimer’s disease, and if this ‘neuronal unrest’ could be stopped the disease progression could be halted. Recent evidence proves such network hyper-excitability in Alzheimer’s patients (Verret, L, 2012), and our research focuses on the underlying mechanisms triggering hyperexcitability. We employ 24/7 continuous local field potential recordings and sleep-stage analysis in combination with behavioral analysis in AD knock-in mice to resolve potential alterations that precede and may predict the deposition of Aβ in the brain.