The Bridge between Schizophrenia and Mitochondria (2010.9.29)
Schizophrenia is a severe mental disorder that entails hallucinations and delusions, for those who suffer it become incapable of controlling their minds. According to existing studies, the cause can be defined through genetic and environmental factors where the role of the gene called ‘Disrupted-in-schizophrenia 1’ has become central in the research. DISC1 in short, implies that this specific gene is found disrupted only in those who suffer from schizophrenia. Management of the disorder depends largely on medications and psychological interventions, but unfortunately, there is no definite cure up to now.
Yet recently, a research team at POSTECH has set forward a novel approach to curing schizophrenia. The team, led by Professor Sang Ki Park at the Department of Life Science, including Post Doctorate researcher Young-Un Park and PhD candidate Jaehoon Jeong, introduced their work on the interaction between DISC1 and mitochondria, and presented a new approach to the cure of schizophrenia. The journal Proceedings of the National Academy of Science USA (PNAS) published Professor Park’s work online on September 28.
A mitochondrion is a membrane-enclosed organelle that can be described as the energy-producer of cells. Mitochondira can be viewed as ‘cellular power plants’ that generate most of the cell’s supply of ATP (Adenosine triphosphate), which is their source of chemical energy. Thanks to this conversion that result in ATP, cells are provided with a usable form of energy, which enables them to function properly.
Professor Park’s research team is the first to reveal the phenomenon that the gene responsible for schizophrenia has a direct impact on the regular behavior of mitochondria. If the DISC1 protein has a problem in functioning, the mitofilin, which is a mitochondrial inner membrane protein, becomes disturbed. Such an event hinders the functioning capacity of mitochondria and can also influence the metabolisms of neurotransmission such as dopamine, a neurotransmitter that results in excitement or agitation in brain cells. Based on this, the team was able to deduct that in order for the mitochondria to function properly, it is necessary for the DISC1 protein to control the mitofilin.
Their discovery explains how schizophrenia can be caused by a functional disorder of mitochondria and how it results in the abnormal behavior of nerve cells. Moreover, Professor Park’s team has come forth with a novel approach instead of working on the mechanism for the cytoplasm of DISC1 proteins as conventionally done.
As Professor Park remarked, the neurobiological explanation for the cause of schizophrenia has been insufficient because the disease requires a high rate of hospitalization, thereby incurring high medical and social costs. Therefore, his team’s novel approach to developing therapeutics for schizophrenia through the manipulation of mitochondria is particularly attractive.