Selenium (Se) is an essential trace mineral mediating its biological function primarily through selenoproteins. Accumulated lines of evidence indicate important roles of selenoproteins in the maintenance of optimal brain functions via redox regulation. Decreased expression of several selenoproteins is associated with the pathologies of a few age-associated neurodisorders, including Parkinson's disease, Alzheimer's disease and epilepsy. Recent advances using genetically manipulated mouse models demonstrate that selenoproteins offer protection against neurodegeneration primarily through redox regulation. Therapies targeting specific selenoproteins influencing redox regulation could delay the onset of neurodisorders, improve quality of life of patients already affected, and perhaps rescue patients with certain diseases by using novel gene therapies.