For decades, scientists have known that chronic exposure to high concentrations of the metal manganese can cause movement abnormalities resembling symptoms of Parkinson’s disease, but apparently without the same neuron damage characteristic of Parkinson’s patients. Now, researchers from the Johns Hopkins Bloomberg School of Public Health and Thomas Jefferson University have discovered a potential explanation to why these neurological symptoms may occur with manganese exposure. The study found that dopamine neurons in the brain of animals exposed to manganese do not release dopamine when stimulated, suggestive of a dysfunctional dopamine system even though the neurons do not show the damage present with Parkinson’s disease. Dopamine is a key neurotransmitter necessary for normal motor function. In addition, the researchers found that effects of manganese exposure occurred at blood concentrations in the upper range of levels documented in children and adults with environmental or occupational exposure. The study is published in the online version of the journal Experimental Neurology.
