Grant: CIHR Fellowship

Schizophrenia (SCZ) is a leading cause of disability world-wide with annual societal costs in Ontario alone estimated to be over $2.1 billion. Genetic research is making great strides to improve diagnosis and treatment, with large, ground-breaking genetic studies in SCZ. However, these major studies did not include the investigation of mitochondrial DNA or epigenetic information. This approach is understudied in SCZ, despite the success seen in cancer research where epigenetics is being used in tests and treatments to save lives. Research in psychiatry remains a decade behind the advanced approaches currently used in cancer studies. Each of our cells has two kinds of DNA, that talk to each other. One type is in the chromosomes and the other is in the mitochondria. This communication is thought to occur via attachments to our DNA called epigenetic marks that can turn our genes on and off. Mitochondria are the energy factories of our cells, and we know that mitochondrial DNA is damaged in SCZ. The damage is thought to be due to excessive stress on the mitochondria's ability to produce energy and control inflammation. We also know that SCZ individuals have different epigenetic marks than healthy individuals. Thus, we will investigate the communication between the two kinds of DNA using epigenetics to clarify the link. We will learn how the communication takes place in healthy individuals and how it is impaired in SCZ. As this is one of the first studies using this strategy in psychiatry, we hope to discover the genes involved in the cross-talk that are impaired in SCZ. Understanding the biology involved in SCZ can lead to understanding the mechanisms and developing biomarkers to be used in early diagnosis, prediction of illness severity, and to create new treatments. This work has the potential to revolutionize personalized medicine in SCZ, improving quality of life for patients and their families and providing substantial economic, societal, and health benefits.