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Parkinson's could be slowed with existing drug
Monday August 10, 2015
Medical News Today - Researchers have discovered a drug that has long been used to treat liver disease could also be used to slow down the effects of Parkinson's disease.
Ursodeoxycholic acid (UDCA) had beneficial effects on fruit fly nerve cells with mutations in the LRRK2 gene - the most common inherited cause of Parkinson's disease.
The study was conducted by researchers from the Sheffield Institute of Translational Neuroscience (SITraN) and the University of York - both in the UK. Their work is published in Neurology.
"We demonstrated the beneficial effects of UDCA in the tissue of LRRK2 carriers with Parkinson's disease as well as currently asymptomatic LRRK2 carriers," states study author Dr. Heather Mortiboys of SITraN. "In both cases, UDCA improved mitochondrial function as demonstrated by the increase in oxygen consumption and cellular energy levels."
Mitochondria give cells the energy they need to carry out their jobs. Defects in mitochondria such as those caused by the LRRK2 gene mutation lead to reduced energy levels that can contribute toward the development of several diseases affecting the nervous system. These include motor neuron disease and Parkinson's disease.
According to the National Institute of Neurological Disorders and Stroke (NINDS), at least 500,000 people are estimated to have Parkinson's disease in the US. The disorder is characterized by shaking limbs, particularly when the body is at rest, along with slow movement. Symptoms typically get worse over time.
Approved drug could save years of research
Dr. Oliver Bandmann, professor of movement disorders neurology at the University of Sheffield, explains the wider implications for their research:
"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. 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."
In fruit flies, the effects of LRRK2 gene mutation on mitochondria can be tracked through the loss of visual function. The researchers fed flies carrying the LRRK2 mutation with UDCA partway through their lives and found that the drug managed to preserve their visual response.
Dr. Chris Elliott, from the University of York, explains that the UDCA treatment demonstrated a marked rescue effect on neural signaling:
"Feeding the flies with UDCA partway through their life slows the rate at which the fly brain then degenerates. Thus, mitochondrial rescue agents may be a promising novel strategy for disease-modifying therapy in LRRK2-related Parkinson's."
Dr. Bandmann states that because UDCA has been in clinical use for decades, it could be brought forward to treat Parkinson's disease quickly if it proves beneficial in clinical trials. As the drug is already approved to treat other conditions, its use could save significant amounts of time and money in research.
The study was partly funded by Parkinson's UK- a charity for supporting people with the neurological condition. The charity's director of research and development, Dr. Arthur Roach, describes the findings as "particularly encouraging," and that the need for new treatments for the disease is urgent.
"This type of cutting edge research is the best hope of finding better treatments for people with Parkinson's in years, not decades," he says.
Last month, Medical News Today reported on a breakthrough study that identified two existing antimalarial drugsthat showed promise in protecting the brain against the progression of Parkinson's disease.
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