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Liver disase drug could slow progression of Parkinson's

Brain degeneration was slowed in fruit flies with the same genetic mutation that causes Parkinson's in humans when they were given the drug UDCA.

By Stephen Feller
Picture A shows a patient without Parkinson's disease and Picture B shows a patient with Parkinson's disease. Photo by University of Sheffield
Picture A shows a patient without Parkinson's disease and Picture B shows a patient with Parkinson's disease. Photo by University of Sheffield

SHEFFIELD, England, Aug. 10 (UPI) -- A drug used for liver disease was found in a study with fruit flies to slow the progression of Parkinson's disease.

Researchers said the drug ursodeoxycholic acid, used to decrease acids that play a role in liver disease, addresses a mutation of the LRRK2 gene, the most common inherited cause of Parkinson's disease.

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The LRRK2 mutation leads to problems with mitochondria, the part of a cell that produces its energy. The reduced energy of cells is a factor in several diseases of the nervous system, including Parkinson's -- though exactly how that leads to the disease remains unclear, researchers said.

"We demonstrated the beneficial effects of UDCA in the tissue of LRRK2 carriers with Parkinson's disease as well as currently asymptomatic LRRK2 carriers," said Dr. Heather Mortiboys, a Parkinson's UK senior research fellow at the University of Sheffield, in a press release. "In both cases, UDCA improved mitochondrial function as demonstrated by the increase in oxygen consumption and cellular energy levels."

Researchers first tested the drug in lab dishes, finding that UDCA had a positive effect on mitochondrial function, leading them to move to testing it on a live model.

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The researchers fed UDCA to fruit flies with the LRRK2 mutation. In fruit flies, the effects of the mutation slowly decrease visual function, allowing researchers to measure the progression of disease. They found when flies with the mutation received the drug, the degeneration of their brains was slowed.

"Whilst we have been looking at Parkinson's patients who carry the LRRK2 mutation, mitochondrial defects are also present in other inherited and sporadic forms of Parkinson's, where we do not know the causes yet," said Oliver Bandmann, a professor of Movement Disorders Neurology at the University of Sheffield. "Our hope is therefore, that UDCA might be beneficial for other types of Parkinson's disease and might also show benefits in other neurodegenerative diseases."

The study is published in Neurology.

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