Alzheimer’s disease (AD) has a multifactorial etiology which includes, among others, vascular dysfunction and aberrant neuroimmunity. We aim to investigate the gene ABI3 as a potential connection between these two facets of AD pathophysiology. Through transgenic murine models, and using a combination of biochemical, immunohistochemical, and in vivo imaging techniques, we will explore how the late-onset AD risk variant S209F ABI3 affects neurodegeneration, immune fitness, and vascular dynamics.

Rare genetic disorders lead to a failure to produce enough blood cells that are frequently fatal, seen most often among young children. These diseases are primarily monogenic, caused by the loss of function in a single gene. To investigate the effects of this loss of function, my project seeks to mimic it outside of the human body, specifically in human bone marrow organoids (BMOs). By studying BMOs, the aim is to identify critical factors contributing to bone marrow failure and ultimately use this information to develop new diagnostic methods.

Star clusters used to be considered to consist of stars that all formed simultaneously and with the same elemental abundances. The surprising discovery that these clusters contain multiple populations with characteristic abundance inhomogeneities remains an enigma. I will investigate whether rotational mixing is a plausible culprit, using massive emission-line stars as tracers of rapid rotation. Also, I will assess the validity of certain light elements as signatures of multiple populations.

DNA nanotubes are widely used as a mimic for cytoskeletal filaments in bottom-up synthetic biology. Using a synthetic starPEG construct that acts as a crosslinker, we succeed in bundling the few nanometer thick DNA nanotubes. In bulk they self-assemble into micron-scale rings. We achieve their contraction upon temperature increase or molecular depletion with crowing molecules such as dextran (in collaboration with Kierfeld group, TU Dortmund).