Innate immunity, TREM2 and Alzheimer’s disease
Alzheimer’s disease is a neurodegenerative disorder and the most common cause of dementia. Aggregation and deposition of amyloid-β (Aβ) and tau lead to senile plaques and intracellular neurofibrillary tangles (NFTs) in certain brain regions. Human genetics suggests that these processes are involved in mechanisms of disease. Recent genetics argue that also innate immunity and lipid metabolism are relevant to the pathogenesis. Mutant variants of TREM2, a receptor expressed by microglia in the brain seem to increase disease risk by loss-of-function.
Our goal is better understanding how innate immunity and TREM2 gene regulate pathological phenotypes of Alzheimer’s disease like amyloid deposition. Better understanding mechanisms of disease is of great importance to drug target identification.
To establish and work with a slice-based tissue model of Alzheimer’s disease as a means to explore effects of intervening in different pathways that are relevant innate immunity and neuroinflammation. Provided funding availability, the project can be further developed as a PhD project. The model system can also come to use for testing effects of drug candidates.
You will gain experience working with mice models of Alzheimer’s disease, cultivating organotypic slice cultures, immunohistochemistry, protein biochemistry including ELISA, SDS-PAGE and Western blot. Molecular biology techniques like PCR will be used.
Lars Nilsson’s research group is located at the Department of Pharmacology, Faculty of Medicine at Rikshospitalet, Oslo.
The candidate will work together with experienced colleagues.