SNCA and Alzheimer disease: In this context, we observe that genetic predispositions, initial elevations in cholinergic activity, excessive calcium influx causing glutamate toxicity, heightened NMDA and AMPA receptor sensitivity, overactivation of mTOR, disruptions in calcium homeostasis due to Aβ, tau, and α-synuclein, hyperstimulation of microglia and astrocytes, and GABA dysfunction collectively contribute to the promotion of hyperexcitability in AD and DLB.