During my PhD training I investigated the role of inflammation in Alzheimer’s disease and especially the mechanism on how nonsteroidal anti-inflammatory drugs (NSAIDs) could lower the risk of developing Alzheimer’s disease. I was one of first to discover that the enzyme cyclooxygenase 1, a primary target of NSAIDs, is expressed in microglia in the human brain. As postdoc researcher I was involved in several projects investigating the molecular mechanism of neurodegeneration in Alzheimer’s disease. During this period, I got interested in regulation of protein folding in neurodegenerative diseases. Using post mortem brain tissue, I was the first to show that the unfolded protein response (UPR) is activated in Alzheimer’s disease. In following studies, I was able to show that the UPR is activated in early stages of Alzheimer’s disease and Parkinson’s disease and show the connection between UPR activation and the accumulation of tau and alpha-synuclein in the human brain. Publications that resulted from these studies are currently recognized as key papers subscribing the role of the UPR in neurodegeneration. Currently I am leading several research projects on protein misfolding and neuroinflammation, as well as on the identification of new biomarkers and drug targets for neurodegenerative disease.