The picture emerges that many brain disorders are to be considered ‘synaptic diseases’ or ‘synaptopathies’, which result from alterations in the molecular and cellular function of synapses.
At the basis of synaptic function is a collection of at most a thousand of different synaptic proteins (the synaptic proteome) that physically interact to form plastic signalling networks (the synaptic interactome). Synaptic function and the plastic changes thereof rely on the specific (changes in) physical interactions between the proteins of the synaptic interactome. Likewise, it is thought that ‘synaptic diseases’ are caused by perturbations in the synaptic interactome that interfere with proper synaptic functioning.
In order to develop effective therapies for synaptic diseases it is imperative that the architecture and dynamics of the synaptic interactome are revealed and the disease-causing changes in the interactome are identified. The key objective of this Research Team is to provide a qualitative/quantitative description of the (extra-) synaptic interactome and to generate quantitative dynamical models of selected ‘hubs’, such as the AMPA receptor (AMPAR).
Team 2.1 Student: Nikhil Pandya / Supervisor: Prof. Guus Smit
Team 2.2.Student: Juan Carlos Valenzuela Macaya / Supervisor: Prof. Eckhardt Gundelfinger
Team 2.3 Student: Christian Seeger / Supervisor: Prof. Helena Danielson