November 21, 2014
New research from the University of Texas at Austin may help unlock the secrets of parkinsonism disorders, such as Parkinson’s disease. Assistant professor of pharmacology and toxicology Somshuvra Mukhopadhyay, M.B.B.S., Ph.D., led a team that studied a mutation in the SLC30A10 gene, which may play a critical role in causing or facilitating parkinsonism.
Published in the Oct. 15, 2014 edition of The Journal of Neuroscience, the researchers found that SLC30A10 inhibits the normal function of affected cells. The protein that is affected by this mutation typically works to manage the levels of manganese within the cell. However, this mutation allows for higher levels of manganese to build up.
Scientists have known that Parkinson’s disease, which affects about 10 million people in the world, is caused by a combination of environmental and genetic issues. Manganese is a major environmental cause of this condition, the university explained.
“Exposure to the metal manganese is an environmental factor known to cause parkinsonism in humans,” the university’s communication office explained. “Manganese-induced parkinsonism is most often seen in individuals with documented exposures to manganese. Exposures may originate from occupational sources such as in welding and mining professions; through environmental sources such as consuming tainted drinking water and food sources; and as a result of disease such as cirrhosis of the liver and alcoholism, which block manganese excretion.”
Mutations in the SLC30A10 gene, which were discovered among Europeans with hereditary Parkinson’s disease, allow for manganese to build up to unsafe levels in the body, akin to environmental exposure.
The researchers explained that “efflux therapy” that counteracts this mutation and facilitates the gene’s normal function may help treat patients with genetic and environmental parkinsonism.
Mitochondrial fission treatment may play role in Parkinson’s disease treatment
Another new study on Parkinson’s disease may help lead to treatments for the condition. Researchers from Plymouth University in the U.K. published their finding in the Nov. 5, 2014 issue of Nature Communications.
Through experiments on mice, the researchers were able to block the mitochondrial fission protein GTPase dynamin-related protein-1 or Drp1. People who have Parkinson’s disease experience the death of brain cells that produce dopamine, which creates difficulty for cell communication and movement control. By stopping Drp1, the number of cells that died in the mice with Parkinson’s disease was reduced and the overall level of dopamine didn’t drop.
“Our findings show exciting potential for an effective treatment for PD and pave the way for future in-depth studies in this field. It’s worth noting that other researchers are also targeting this mitochondrial fission/fusion pathway as potential treatments for other neurological diseases such as Alzheimer’s disease, Huntington’s disease and Amyotrophic Lateral Sclerosis,” said study researcher Kim Tieu, Ph.D.