The drug levodopa and most other therapies developed over the years for Parkinson’s disease have been centered on correcting the lack of dopamine. Researchers acknowledge that the reason dopamine producing neurons die is still unknown.
According to Parkinson’s News Today, a new study is taking a proactive approach. It is focusing on developing a treatment to prevent the loss of dopamine producing neurons (dopaminergic) rather than trying to replace missing dopamine.
A major breakthrough occurred with the recent discovery that abnormal cellular mechanisms occur in certain groups of Parkinson’s disease patients.
Identifying the differences in these diseases and assessing treatments that protect the neurons (neuroprotective) in each instance opens the door to personalized therapies.
About Parkinson’s Disease
Parkinson’s disease is characterized by the loss of neurons that produce the neurotransmitter dopamine (dopaminergic). It is a progressive nervous system disorder (neurodegenerative) where the loss of dopamine will result in a range of symptoms such as impaired balance and tremors or excessive mood swings.
About the Study
Skin biopsy samples were taken from one hundred Parkinson’s patients by researchers at the University of Sheffield, United Kingdom.
The team discovered that there were two groups in the study that exhibited distinctly different functions of their lysosomes or mitochondria.
Lysosomes break down potentially toxic molecules and mitochondria provide the cells with energy. Malfunction of either causes nerve death, contributing to Parkinson’s symptoms.
ATP is a molecule that is produced by the mitochondria. It is of interest that some Parkinson’s patients produced less ATP than other patients or healthy individuals in the control group.
Yet certain Parkinson’s patients had significantly more lysosomes compared to the healthy controls and other Parkinson’s disease patients.
Ursodeoxycholic Acid (UDCA)
UDCA’s current application, treating liver disease, has been in use for over three decades.
Researchers screened over two thousand drugs and identified UDCA as having the highest potential to affect mitochrondrial function in Parkinson’s disease.
The research team was able to test the UDCA compound working directly within the patients’ dysfunctioning mitochondria.
Previous research indicates that UDCA aids in the function of mitochondria by preventing dysfunctional mitochondrial cells from dying. This gives rise to the possibility of UDCA slowing or even halting the progression of Parkinson’s disease.
Researchers are conducting a Phase II clinical trial (NCT03840005 ) that is investigating the tolerability and safety of the drug. Another critical endpoint is to assess whether UDCA can slow down the progression of Parkinson’s disease.
Oliver Bandmann, professor of neuroscience at Sheffield Institute, commented that if this first trial of UDCA is successful, it will lead to a much larger study to establish the drug as a treatment that impacts Parkinson’s progression.