For our first WCMR Science Seminar of 2022, we heard from PhD student Jane Tweedy about her research project that investigates mitochondrial shape in Parkinson’s disease as part of the MRC Discovery Medicine North Doctoral Training Partnership (DiMeN). Read on to find out more.
Approximately 10 million people worldwide suffer with Parkinson’s disease, a condition that most commonly affects people over 60 years of age. Parkinson’s disease results from the loss of brain cells that produce a chemical called dopamine. The main symptoms are slowness of movements, tremors, impaired balance, and stiffness. These symptoms gradually develop over-time as the dopamine-producing brain cells are lost.
What drives the loss of these dopamine-producing brain cells?
While the exact cause for their loss is unknown, a part of the cell known as mitochondria may play an important role. The brain and the dopamine-producing cells are highly energy consuming. Mitochondria provide energy from the food we eat so that our cells can perform many duties. To meet the cell’s requirements, mitochondria continually change shape. In previous research of Parkinson’s disease, it was found that mitochondria provide less energy and there are fewer shape changes. Their shape has been shown to become small and round compared to more branched shapes in control cells. However, this has not been investigated in three-dimensional (3D) pictures or in human brain cells.
I want to investigate how the 3D shape of mitochondria differs in people with Parkinson’s disease.
I will look at the dopamine-producing cells in human brain tissue using precious samples kindly donated to research by people who lived with Parkinson’s disease. The brain cells are scanned in layers so we can see the tiny structures in the cell that are invisible to the naked eye. The resulting images are then used to produce coloured 3D reconstructions of the mitochondria as shown below:
There is currently no cure for this devastating problem, only medicines that may provide some relief from the symptoms experienced above. This work will help us understand in more detail how mitochondria change in Parkinson’s disease. I anticipate this will eventually enable the development of new drug treatments that target the mitochondria, for example, treatments that restore mitochondrial shape.