Yao found that Neuronal hyperactivity is an early primary dysfunction in Alzheimer’s disease (AD) in humans and animal models, but pharmacologically limiting RyR2 open time with the R-carvedilol enantiomer prevents and rescues neuronal hyperactivity, memory impairment, and neuron loss even in late stages of AD [32]. The gene discussed is RYR2; the disease is Alzheimer disease.