Neuroinflammation is a common hallmark in e.g. amyotrophic lateral sclerosis (ALS), fronto-temporal dementia (FTD) and Alzheimer’s disease (AD). AD is characterized by the accumulation of extracellular amyloid-beta (Aβ) in amyloid plaques and intracellular tau in neurofibrillary tangles (NFTs).
Activation of microglia, the innate immune cells of the brain, seems to be involved in the development and progression of these pathologies in AD but also plays a role in other neurodegenerative diseases. To date, the underlying mechanisms in the transition of an initially protective to a chronic, harmful neuroinflammatory response are unknown.
Our basic laboratory research aims at understanding molecular mechanisms of inflammatory regulation in a variety of neurodegenerative disease by using for example novel preclinical mouse models and state-of-the-art techniques like two-photon imaging, transcriptome analysis and induced pluripotent stem cells (iPSCs).
Current clinical research is focused on various aspects of neuroinflammation involved in neurodegenerative and cerebrovascular diseases with the goal of developing new biomarkers and medical intervention programs.