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My main research focus has been on microglia (brain macrophages) and their role in neurodegenerative diseases. Work from my lab has already contributed significantly to our understanding of how microglia contribute to Alzheimer’s disease (see e.g. Varvel et al., J. Exp. Med., 2015; Wendeln et al., Nature, 2018). In particular, our publication in Nature described a novel concept in the field of neuroimmunology, namely the capacity of microglia for immune memory. Notably, this innate immune memory in the brain was sufficient to modify neurological disease. We further demonstrated that microglial immune memory was driven by epigenetic mechanisms, which have received relatively little attention in neuroinflammation research. Current projects in the lab are aimed at understanding the molecular mechanisms of microglial immune memory at the single cell level.
Recently, I have developed another area of interest, namely vascular dysfunction during aging and AD, driven by medin amyloidosis. Medin amyloid is the most common human amyloid known to date, but has received little attention. This is, because its pathological impact remained unknown until my lab recently reported that medin aggregation contributes significantly to age-associated dysfunction of brain blood vessels (Degenhardt et al., PNAS, 2020). Current projects are focusing on the possible contribution of medin amyloid to neurodegenerative diseases.