Identification of Cellular Targets for Amyloid Beta Toxicity in Alzheimers Disease

Important results from the project

The aim of the project has been to improve molecular and mechanistic understanding of how amyloid beta aggregates mediate Alzheimer´s disease. The project has resulted in several peer-reviewed publications, mainly concerning cell interactions of amyloid aggregates and improved fluorescence methods for their detection. The project has also fulfilled the goal of providing career opportunities for Elin Esbjörner who today has an established research group at Chalmers and has become promoted to Associate Professor (docent).

Expected long term effects

This project has resulted in better understanding of how amyloid-beta aggregates interact with cells and biomimetic membrane models (liposomes). We have explored endocytic mechanisms for amyloid-beta cell entry and shown how cell membrane like lipid vesicles can catalyse the formation of amyloid beta fibrils. The project outcome has inspired continued studies in my lab directed towards establishing structure-activity relations for the uptake of amyloid proteins in different aggregated forms.

Approach and implementation

This project has been performed by my research group at Chalmers, but also as a collaborative project with SLU and Uppsala University involving research groups there. Initially I spent time in Uppsala, performing experiments in two labs and learning new techniques. This also provided important opportunity to experience a different Swedish research environment than that at Chalmers. As the project has progressed and my research has become more well established at Chalmers, the project has shifted towards my lab. By the end of the project, one PhD student and one postdoc were involved.