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.
Gallium manganese arsenide incorporated. At lower temperatures, around 250 °C, there is insufficient thermal energy for surface segregation to occur but still sufficient for a good quality single crystal alloy to form. In addition to the substitutional incorporation of manganese, low-temperature MBE also causes the inclusion of other impurities. The two other common impurities are interstitial manganese and arsenic antisites. The former is where the manganese atom sits between the other atoms in the zinc-blende lattice structure and the latter is where an arsenic atom occupies a gallium site. Both impurities act as double donors, removing the holes provided by the substitutional manganese,