Has the culprit of Parkinson's disease been found?
Key role in brain cell death in Parkinson's disease
genetic mutations can play a role
LifeSciencesToday based on UCL news: Genetic mutations linked to Parkinson's diseaseBritish scientists have established how genetic mutations associated with Parkinson's disease can play a key role in the death of brain cells.
This discovery paves the way for the development of more effective medicines.
In an article published in the journal Nature Neuroscience (Burchell et al., The Parkinson's disease-linked proteins Fbxo7 and Parkin interact to mediate mitophagy), a group of scientists from University College London (UCL), the University of Cambridge (University of Cambridge) and the University of Sheffield (University of Sheffield) describes how defects in the Fbxo7 gene associated with Parkinson's disease lead to problems with mitophagy – the most important process by which our body gets rid of damaged mitochondria.
Cellular organelles of mitochondria are the "power plants" of cells that produce energy for them. For neurons, which require a particularly large amount of energy to perform their functions and survive, the normal functioning of mitochondria is vital. Damaged mitochondria can cause significant harm, and usually cells are freed from dysfunctional mitochondria by "eating" them. This process is called mitophagy.
Most of the knowledge about the process of mitophagy was obtained in the study of familial forms of Parkinson's disease – one of the most common diseases of the brain. Studies of the last three years have proved that two genes associated with the familial form of Parkinson's disease, PINK1 and Parkin, play a certain role in mitophagy.
A new study by British scientists shows how important the role of mitophagy is and how mutations in the Fbxo7 gene are associated with the disease and disrupt the PINK1-Parkin molecular pathway. In patients with Parkinson's disease, genetic mutations disrupt the mitophagy process, leading to the accumulation of dysfunctional mitochondria. This may explain, at least in part, the death of brain cells in patients with these mutations.
"The data we have obtained suggest the possibility of developing therapeutic strategies focused on mitophagy in the future," says one of the lead authors of the article, Dr. Helene Plun–Favreau from the UCL Institute of Neurology. "What makes the results of this work so valid is the confirmation of defective mitophagy on a number of different models of Parkinson's disease, including cells of patients with mutations in the Fbxo7 gene."
"This study draws the attention of scientists studying Parkinson's disease to the importance of maintaining normal mitochondrial function for the health of neurons. In fact, we have just started this work, but perhaps we will be able to use the information obtained for early diagnosis of Parkinson's disease or for the development of treatments aimed at preserving the viability of mitochondria," says her co–author Dr. Heike Laman from the University of Cambridge.
"This study raises interesting questions about exactly how brain cells die in patients with Parkinson's disease, that is, about the process that is the key to understanding the progression of the disease. The deeper we understand the main molecular events that contribute to the onset and progression of Parkinson's disease, the more advantageous the development of treatments that stop this disease will begin," commented Professor Hugh Perry, Chairman of the Council on Nervous Diseases and Mental Health (Neurosciences and Mental Health Board). Medical Research Council.
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