Alzheimer's disease/neuropharmacology

Lars Nilsson<br>Group leader
Lars Nilsson
Group leader

Research aims

Alzheimer’s disease (AD), the most common cause of age-related dementia, is a major societal problem due to the lack of efficacious therapeutics. Central to AD-pathogenesis is amyloid-β aggregation and plaque deposition in the brain. Such deposits also contain other constituents like heparan sulfate proteoglycans. Genetics has for long been centered on amyloid-β but recently risk factor genes have been linked to innate immunity. Interestingly one of them, TREM2, has been linked to several neurodegenerative disorders including Alzheimer’s disease. The aim of our study is to dissect immune-based mechanisms which impact on amyloid-aggregation, and to exploit such pathways for therapeutic intervention.   

Current projects

• Developing a drug for Alzheimer’s disease by targeting the TREM2-receptor
• Explore the biomarker potential of cerebrospinal fluid soluble TREM2-fragments
• Investigate TREM2-biology in AD using cell culture models, organotypic brain slice cultures and transgenic mice models
• Study effects of peripheral inflammation on AD neuropathology in the context differences in heparan sulfate structure

Contact information:
Group leader Professor Lars Nilsson Department of Pharmacology University Oslo/Oslo University Hospital Postboks 1057 Blindern NO-0316 Oslo, Norway.
Tel: +47 22840221, E-mail: