In an earlier article, I discussed Parkinson’s disease (PD) and its devastating implications. To summarize, PD is a neurodegenerative brain disorder that leads to a gradual halt in the production of the neurotransmitter dopamine. As dopamine levels drop, individuals lose control of their ability to regulate body movements and emotions. While PD itself is not fatal, complications that arise from the disease are extremely serious.
Pioneering research led by academics from the Sheffield Institute of Translational Neuroscience (SITraN), in collaboration with scientists from the University of York, supports the notion that the drug ursodeoxycholic acid (UDCA), which has already been in use for decades to treat liver disease, should be fast-tracked for a clinical trial in patients with PD.z
Dr. Heather Mortiboys, a Parkinson’s UK Senior Research Fellow, 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. In both cases, UDCA improved mitochondrial function as demonstrated by the increase in oxygen consumption and cellular energy levels.”
First, let’s take a step back and explain what this all means. A mutation in leucine-rich repeat kinase 2 (LRRK2), known as the G2019S mutation, is the greatest known contributor to PD. Although PD is typically viewed as an idiopathic condition, insinuating that we simply do not know the cause of the disease, roughly 10% of PD cases have been linked to genetic causes. Therefore, by studying LRRK2, we can speed progress towards treatments that would benefit everyone with the disease, not just those with this genetic mutation.
Image Source: Michael Blann
This study has shown that the drug UDCA increases the productivity of the tissue containing these LRRK2 carriers, as demonstrated in the spike in cellular energy levels. Cells are the building blocks of tissue, and one manner in which the productivity of a certain tissue can be measured is through the activity of its constituent cells. This, in turn, was measured from the activity level of these cells’ mitochondria, which was measured through the amount of oxygen consumed. In this way, it was demonstrated that the tissue containing LRRK2 carriers increased their productivity after administration of the drug UDAC.
What does this, however, have to do with Parkinson’s? In what way can a drug utilized for liver treatment help a neurodegenerative disease? Find out in the next article Promising New Drug for Parkinson’s Disease: Part II!
Feature Image Source: “Parkinson’s Volunteers.” by Sebastian.gone.archi is licensed under CC BY-NC 2.0
