An issue in the cell disposal system, which keeps the mitochondria of brain cells healthy, could be contributing to the development of Parkinson’s disease. Research from the University of Nottingham has found a link between issues in the cell’s disposal system and faulty mitochondria, which could add to the death and dysfunction of brain cells.
The study, helmed by Dr. Lynn Bedford of the University of Nottingham’s School of Life Sciences, used gene targeting techniques in mice and found that a damaged ubiquitin proteasome system in neurons can contribute to faulty mitochondria, which produce less energy. The ubiquitin proteasome system, or UPS, functions as a waste disposal system that removes any unneeded proteins from the cells to help them continue to function normally. When this system is damaged, it causes damage to the cell’s mitochondria, which can result in the production of molecules that cause harm to the cell in the form of oxidative stress. The study also showed that when the neuron’s UPS was damaged, the faulty mitochondria were not removed from the cell as they would normally be, leaving them in place and causing damage.
Dr. Bedford stressed the need for a cell’s UPS to be functioning correctly, as without removal, waste can build up and become toxic, resulting in eventual cell death. Neurons are responsible for transferring information throughout the brain, and the death of these cells is one of the causes of neurodegenerative diseases such as Parkinson’s and Alzheimer’s. Dr. Bedford commented on the findings, stating “The study highlights the importance of the ubiquitin proteasome system (UPS) for healthy mitochondria.”
This research encourages a better understanding of the inner workings of brain cells and what can cause them to die as we age. Further studies may target the ubiquitin proteasome systems in neurons and assess their functioning ability, with the goal being reparation that can prevent the build-up of waste and hopefully slow the progression of neurodegenerative diseases.
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