Does Manganese Contribute to Methamphetamine-Induced Psychosis?

Purpose of Review This review describes the increasing global problem of methamphetamine (MA) use and development of psychosis, the molecular and structural basis for this form of psychosis, and its treatment. The putative contribution of manganese (Mn), a common element found widely in nature and industry, to the development of MA-induced psychosis is discussed in relation to its shared toxicity with MA. Recent Findings Both MA and Mn cause damage to brain monoaminergic, glutaminergic, and GABAergic systems and to the blood brain barrier, leading to higher exposure to Mn. Iron (Fe) deficiency can also lead to Mn overexposure. Polymorphisms for genes encoding metabolic enzymes and transport proteins increase risk of toxicity and development of psychosis. Impaired hepatic Mn excretion from viral hepatitis also risks Mn toxicity. It is possible that potential synergistic and/or additive effects of Mn in concert with MA may worsen, prolong, or shorten onset of psychosis.