In this review, we explore shared and distinct molecular mechanisms associated with hyperexcitability in AD and DLB, encompassing factors such as genetic risk factors, Ca2 and glutamate contributions, cholinergic pathways, AMPA and NMDA receptors, mTOR, pathological Aβ, tau and α-synuclein, genetic risk factors, altered microglial and astrocytic activity, and impaired inhibitory interneuron function (Figure 1). This evidence concerns the gene MTOR and Alzheimer disease.