A new study finds that the inhibition of a particular mitochondrial fission protein, GTPase dynamin-related protein-1 – Drp1, could hold the key to treating Parkinson's Disease.

Parkinson's Disease  is a progressive neurological condition that affects movement. 60,000 Americans are diagnosed with Parkinson's each year but there is no cure and little understanding of why some people get the condition. 

Research has found that the debilitating movement symptoms of the disease are primarily caused by the death of a type of brain cell that produces a chemical called dopamine. This brain chemical (also known as a neurotransmitter) helps nerve cells to send signals to other nerve cells.

A reduction in dopamine from cell death results in a lack of communication between nerve cells, which in turn leads to difficulty in movement control. Understanding why these nerve cells die or do not work properly could lead to new therapies.

Mitochondria are small structures within nerve cells that help keep the cells healthy and working properly – they are, in effect, the power generators of the cell. Mitochondria undergo frequent changes in shape, size, number and location either through mitochondrial fission (which leads to multiple, smaller mitochondria) or mitochondrial fusion (resulting in larger mitochondria).

These processes are controlled mainly by their respective mitochondrial fission and fusion proteins. A balance of mitochondrial fission/fusion is critical to cell function and viability.

The research team found that when Drp1 was blocked using either gene-therapy or a chemical approach in experimental models of Parkinson's Disease in mice, it reduced both cell death and the deficits in dopamine release – effectively reversing the Parkinson's Disease process. The results suggest that finding a strategy to inhibit Drp1 could be a potential treatment.

The research team is led by Dr. Kim Tieu from the Institute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry. Tieu said, "Our findings show exciting potential for an effective treatment for Parkinson's Disease 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."

Claire Bale, Research Communications Manager at Parkinson's UK, said, "We've known for decades that problems with mitochondria - the batteries of the cell - play a key role in the death of nerve cells in Parkinson's, but the research in this area hasn't yet led to new treatments. This study, which reveals a potential new drug target to protect mitochondria, is a promising step towards slowing down or stopping the progression of Parkinson's."