Dr. Patrik Verstreken obtained his degree in bio-engineering from the university of Brussels in 1998. He joined the Graduate school of Biomedical sciences at Baylor College of Medicine in Houston, Texas and under the mentorship of Hugo Bellen, he obtained a PhD in Developmental Biology in 2003. After postdoctoral training and with support of a Marie Curie Excellence grant he became a group leader at Vlaams Intituut voor Biotchnologie (VIB) and joined the faculty of the KU Leuven in 2007. Dr. Verstreken obtained an ERC starting grant in 2011 and an ERC consolidator grant in 2015. Since 2017, he has been the director of the VIB-KU Leuven Center for Brain & Disease Research.
Patrik Verstreken has made contributions to the understanding of synaptic function in health and neurodegenerative disease. Using fruit flies and more recently also human neurons derived from embryonic stem cells, his work has focused on key proteins, lipids and mitochondria that regulate synaptic activity and how these molecules and organelles are dysregulated in Parkinson’s disease. Dr. Verstreken’s work has led to the discovery of specific presynaptic and organellar defects in Parkinson’s disease and in strategies as to how these defects can be suppressed.
Sleep defects in Parkinson’s disease occur with high penetrance
Parkinson’s disease affects millions of people around the world. The disease is characterized by typical movement defects that are caused by the loss of dopaminergic neurons, but several very debilitating non-motor symptoms occur more than 10 years before the motor symptoms. I will discuss how we study these non-motor symptoms including sleep disturbances and olfactory defects using large collections of knock in fruit flies that model the numerous familial forms of Parkinson’s disease as well as using human iPS cells from patients. A common emerging theme are defects in protein homeostasis that in specific neuronal cell types, cause cellular defects that explain the Parkinson-relevant phenotypes. Our work reveals the mechanisms that cause early defects in Parkinson’s disease and it opens therapeutic avenues to start tackling this disease.