Research

We want to contribute to a better mechanistic understanding of the cellular processes that cause or mediate the "pathological" elimination of synapses. Learn more

Research area 1

We want to contribute to a better understanding of molecular mechanisms that control synapse stabilization over disassembly. The objective is to identify the molecular mechanisms that cause massive, rapid loss of synapses. In particular we are interested to answer the following questions:

• What (e.g. the lack of a specific protein) makes synapses prone to elimination ?
• Might the misregulation of pathways, normally involved in refining synaptic circuits during learning and memory, set the trigger for massive loss of synapses in neurodegenerative diseases?
• Can inducible impairments in transport can be used to trigger synapse elimination? How accurately can synapse elimination be predicted by measuring axonal transport rates?

Research area 2

The multiplicity of potential functions ascribed to APP and its derivatives in vitro led to the proposal that this protein may be part of several regulatory pathways, and that the disruption of these functions may contribute to the pathology of AD.
Thus, we investigate the mechanisms by which misregulated APP/APPL function leads to pathological events and subsequent symptoms of AD. Studying this effect in vivo allows us to decipher the temporal sequence of cellular events.

Learn more about:
in vivo imaging