The main theme of my research is how our genetic background shapes the influence of the environmental risk for bipolar disorder and schizophrenia.
The idea that psychiatric disorders develop as a result of the interaction between genes and environment is generally supported. However methodological challenges of such studies have limited large scale genome wide efforts. Therefore studies that focus on the interaction between environmental risk and genetic background remain timely and necessary.
However such genetic studies do not take into account a more subtle but highly relevant molecular mechanisms of interactions between environment and genes that recently is identified as a key mechanism of adaptation. These mechanisms, referred to as epigenetics, are extensive and complex and to date not fully understood. Central to our understanding is that epigenetic mechanisms influences transcription of DNA by modifying access to the DNA sequences. What makes this line of research extra interesting is the potential for pharmaceutical manipulation.
To focus these studies we have chosen cannabis and trauma as a main environmental exposure. In addition to genetic variation as a modifier of environmental risk we study gene expression and DNA methylation levels. DNA methylation is central in gene-environment interaction as epigenetic silencing of risk genes is partly under the influence of environmental exposures of the probands as well as the mother. This work is supported by a NARSAD young investigators award and a Neuroscience and Cognition Utrecht stipendium. We are currently conducting a study on the influence of maternal famine in China on schizophrenia risk and investigate epigenetic modification of the stress response in relationship with post-traumatic stress- and bipolar disorder.
Specialties: Psychiatry, epigenetics, genetics, bio-informatics