In agreement with the presented MT-I+II actions, various brain disorders are more severe in MT-I+II deficient mice than in wildtype controls, whilst the clinical and histopathological symptoms are efficiently diminished by MT-I overexpression and exogenous MT-I or MT-II treatment (Aschner and West, 2005; Penkowa et al. 2006a, b). Here, MT2A is linked to brain disorder.