In Alzheimer’s disease, nNOS overactivation exacerbates amyloid-beta-induced oxidative stress, promoting synaptic dysfunction and neuronal death, while in Parkinson’s disease, elevated nNOS activity contributes to dopaminergic neuronal degeneration through mitochondrial damage and neuroinflammation [58,59]. Here, NOS1 is linked to early-onset autosomal dominant Alzheimer disease.