Research focus

​Recently and unexpectedly, several molecules with angiogenic activity have been causally implicated in neurodegeneration, thus revealing an intriguing and very relevant connection between angiogenic factors and neurodegeneration. The first angiogenic factor implicated in neurodegeneration was VEGF. By applying a large number of gene-targeted and experimental animal model systems, we now aim to generate fundamental knowledge on the mechanisms of neurodegeneration and the role of so-called angiogenic factors in those mechanisms. More specifically, we intend to explore whether these angiogenic molecules influence neurodegeneration by acting on the neurovasculature or by acting as pleiotrophic factors, modulating neuro-inflammatory responses and exerting protective effects on neurons. We will also carefully assess the therapeutic potential of these novel molecules in various neurodegenerative models (e.g. motor neuron degeneration and neuropathic models) and assess whether other well-established angiogenic factors play a previously unrecognized role in neurodegenerative disease.

In recent years, innovative technologies have been key in allowing the field of complex genetics to move rapidly forward, so that nowadays genetic studies are providing the basis for many of the major advances in biology and medicine. Indeed, a myriad of genetic and molecular modifications, such as single nucleotide variations (SNPs), epigenetic changes (e.g. DNA methylation) and non-coding RNAs (microRNA), are found to substantially regulate gene expression and to induce a variety of complex human traits and disease diversities.

In the past, the Vesalius Research Centre (VRC) has invested significantly in animal model systems to perform functional genetic studies (zebrafish, tadpoles and mice). However, model organisms do not always reflect what really happens in human disease.

We therefore aim to translate our animal genetic findings into the human realm by generating conclusive genetic evidence in human disease. By applying an opposite strategy, we also aim to identify novel and clinically relevant disease genes, which will then be studied in our classical animal models to unravel the mechanisms by which these genes cause human disease, and also to assess their therapeutic potential.

To this end, a number of collaborations have been initiated with clinicians at the University Hospital in Leuven, and large-scale DNA collections of patients included in clinical trials or databases are currently ongoing.