Hence, changes to neural circuit excitation have traditionally taken a back seat in explaining deviating E/MEG spectra in AD, despite the observation that restoring excitatory activity levels—in computational models—is the most effective treatment for counteracting AD-related frequency slowing [68] and the relative success of cholinesterase inhibitors—the presently available drugs for AD—which promote signal transmission and have been shown to be able to restore alpha rhythms [69]. The gene discussed is BCHE; the disease is Alzheimer disease.