New discoveries place lack of energy at the basis of Parkinson’s Disease
News Mar 24, 2014
Neuroscientists have demonstrated how a defect in the gene Pink1 results in Parkinson’s disease (PD). By mapping this process at a molecular level, they have provided the ultimate proof that a deficient energy production process in cells can result in Parkinson’s disease. The results of their work have been published in the journal Science.
Mitochondria are cell components that produce the energy required by a cell to function. The action of these mitochondria – and therefore the energy production in cells – is disrupted in Parkinson’s disease. The exact mechanism was unknown. In recent years, scientists have described various gene defects (mutations) in Parkinson’s patients that result in decreased activity of the mitochondria, including a mutation in the Pink1 gene.
Vanessa Moraïs studied the link between Pink1, mitochondria and Parkinson’s disease in fruit-flies and mice with a defective Pink1 gene. These model organisms exhibited symptoms of Parkinson’s disease as a result of this defect. She was able to demonstrate that the defect in Pink1 resulted in the so-called ‘Complex I’ – a protein complex with a crucial role in the energy production of mitochondria – not being phosphorylated adequately, resulting in decreased energy production. When Moraïs and her colleagues ensured correct phosphorylation of Complex I, the Parkinson’s symptoms decreased or disappeared in mice and in patient-derived stem cell lines. The scientists thereby demonstrated that the lack of phosphorylation causes Parkinson’s disease in patients with a defect Pink1 gene.
This study reveals that repairing the phosphorylation of Complex I could be a treatment strategy for Parkinson’s disease. The VIB scientists have already used cells from Parkinson’s patients with a defective Pink1 gene to demonstrate that repairing the phosphorylation results in increased energy production. However, will this cause the symptoms of Parkinson’s disease to decrease or disappear? Only tests on patients can answer this question. According to the scientists, the best strategy would be to start with the sub-group of patients with a defective Pink1 gene. But before starting clinical trials, a lot of aspects still have to be tested.
Note: Material may have been edited for length and content. For further information, please contact the cited source.
Vanessa A. Morais, Dominik Haddad1, Katleen Craessaerts, Pieter-Jan De Bock, Jef Swerts, Sven Vilain, Liesbeth Aerts, Lut Overbergh, Anne Grünewald, Philip Seibler, Christine Klein, Kris Gevaert, Patrik Verstreken, Bart De Strooper. . PINK1 Loss of Function Mutations Affect Mitochondrial Complex I Activity via NdufA10 Ubiquinone Uncoupling. Science, Published Online March 20 2014. doi: 10.1126/science.1249161
Neuronal alpha oscillations in the range of 10 Hz are neural waves that reduce processing in certain brain regions to provide resources for upcoming information. Alpha oscillations can be easily influenced by neurofeedback training. Researchers have discovered that participants can self-regulate their learning success in a perceptual learning task by altering their alpha oscillations.READ MORE
Anxiety and depression are surprisingly common among young children. But it can be hard to detect these conditions, known as “internalizing disorders,” because the symptoms are so inward-facing that parents, teachers and doctors often fail to notice them. Now, researchers have developed a tool that could help screen children for internalizing disorders to catch them early enough to be treated.
14th Annual Conference on Dementia and Alzheimer's Disease
Sep 19 - Sep 20, 2019