Manganese produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this Parkinsonism-like disease. The Lewy bodies typical to PD are not seen in Mn-induced parkinsonism. Animal experiments have given the opportunity to examine the consequences of manganese overexposure under controlled conditions.
Manganese dioxide At temperatures of 400 °C, the salt decomposes, releasing and leaving a residue of purified manganese dioxide. These two steps can be summarized as: In another process manganese dioxide is carbothermically reduced to manganese(II) oxide which is dissolved in sulfuric acid. The filtered solution is treated with ammonium carbonate to precipitate . The carbonate is calcined in air to give a mixture of manganese(II) and manganese(IV) oxides. To complete the process, a suspension of this material in sulfuric acid is treated with sodium chlorate. Chloric acid, which forms in situ, converts any Mn(III) and Mn(II) oxides to the dioxide, releasing