Aggregation and deposition of amyloid-β (Aβ) as extracellular plaques and also of intracellular neurofibrillary tangles (NFTs) in the brain leads to neurodegeneration and functional decline by partly unclear mechanisms. Genetics indicate that Aβ-metabolism, the lipid transporter protein Apolipoprotein E (ApoE) and most recently also mechanisms of innate immunity are relevant to AD pathogenesis. Mutations in the innate immune receptor TREM2 represent a strong genetic risk factor for Alzheimer’s disease. TREM2 serves critical functions of microglia, the chief immune response cell of the brain.
Our goal is to develop a drug which affects TREM2-receptor signal transduction and thereby enhances microglial functions in Alzheimer’s disease brain.
Master project:
To establish effective screening systems, identify and characterize Alzheimer’s disease drug candidates that modulate the TREM2 signaling pathway. It will be possible to test treatment effects with drug candidates in a future PhD project, since the group has long-standing experience of working with Alzheimer’s disease mouse models.
Methods:
You will gain experience with sterile cell culture, transfection, eukaryotic protein expression, protein purification, receptor binding assays, ELISA, SDS-PAGE Western blot and Flow Cytometry.
Working place:
The Nilsson group is localized at the Department of Pharmacology, Faculty of Medicine at Rikshospitalet, Oslo.
The candidate will work together with experienced colleagues.
Veileder: Lars Nilsson
Intern veileder: Marianne Fyhn