In Alzheimer’s disease (AD), the most prevalent form of dementia, the aggregation of the amyloid β peptide (Aβ) leads to formation of amyloid fibrils, the major compound of amyloid plaques found in AD patients’ brains. Finding ways to inhibit amyloid-associated toxicity is key to develop efficient therapeutics against amyloid diseases. We work with the Bri2 BRICHOS protein, which inhibits Aβ aggregation, and therefore holds the potential to be implemented in new therapeutic and diagnostic tools.

Our research concerns investigations of Aβ fibril structures in vitro and derived from AD mouse models, since knowledge about molecular fibril structures and translation to the in vivo situation are the basis for design of novel amyloid inhibitors.
Furthermore, we study how the Bri2 BRICHOS protein can modulate Aβ aggregation by binding to the fibril surface. This will give valuable insights on how molecular chaperones can be harnessed for therapeutic applications in AD.

This project involves a broad range of different techniques ranging from protein biochemistry and biophysics to in vivo experiments, and the student projects can be tailored to concern specific parts using biochemical and biophysical methods or/and AD mouse models.

You are most welcome to contact us so that we can discuss the project in detail!