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(II) sulfate highly characteristic. Typically, manganese ores are purified by their conversion to manganese(II) sulfate. Treatment of aqueous solutions of the sulfate with sodium carbonate leads to precipitation of manganese carbonate, which can be calcined to give the oxides MnO. In the laboratory, manganese sulfate can be made by treating manganese dioxide with sulfur dioxide: It can also be made by mixing potassium permanganate with sodium bisulfate and hydrogen peroxide. Manganese sulfate is a by-product of various industrially significant oxidations that use manganese dioxide, including the manufacture of hydroquinone and anisaldehyde. Electrolysis of manganese sulfate yields manganese dioxide, which is called EMD