Research & Faculty
Department of Infectology
Recent years have witnessed a wealth of data showing the implication of the prion protein in disease susceptibility and its contribution to the replication of the prion. However, there are still major areas which need to be deciphered, amongst which:
How does the prion enter into a cell and spread to another one?
Which host factors does it bind to in order to enable its multiplication?
What exactly causes the death of the neurons?
What would be the best approach to impede prion replication?
Block the protein itself or interfere with a ligand?
Is there a way to prevent neuronal death?
Much of our past effort has been dedicated to understand the pathogenesis and the mechanisms of prion transmission from one species to another and its propagation within the body. We also studied the neurotoxic mechanisms and showed, using primary cultures of neurons, that low molecular weight aggregates of the prion protein are neurotoxic. In collaborative studies, we have found that the non integrin laminin receptor can act as a cellular receptor for the prion protein. Our aim now is to devise intervention strategies based on the blockage of the neurotoxic entities on the one hand, and of prion replication on the other hand, using a two step approach in scrapie-infected cells and rodent models of prion diseases.
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