Preclinical studies demonstrate efficacy in models of Alzheimer’s disease, depression, ischemic stroke, and age-related cognitive decline, largely through mechanisms involving anti-tau aggregation, inhibition of monoamine oxidase-A (MAO-A), reduction of neuroinflammation, and regulation of oxidative stress pathways (Rustage et al. 2025). This evidence concerns the gene MAOA and early-onset autosomal dominant Alzheimer disease.