Max Theo Ben Clabbers

My research aims to understand and address health issues related to tiny crystalline structures in cells. These crystallites cause various diseases and form a major concern for public health. Despite their broad impact, we often do not fully understand how they form or affect cellular tissue. Traditional methods typically fall short because the crystals are too small, and samples are studied outside of their natural environment. Our project focuses on improving our understanding of these crystalline pathologies by studying them directly within cells. To achieve this, my research group develops novel methods for in situ electron crystallography that use cryogenic electron microscopy imaging and diffraction to look at these crystals in their natural environment. Specifically, we apply these methods to study crystalline problems associated with type 2 diabetes. Our research will not only benefit diabetes treatment but also pave the way for studying a much broader range of pathologies.

Freja Herborg

Unraveling the complex interactions among neural circuits in the brain is pivotal to advance our understanding of psychiatric disorders and symptoms like social impairments that are common across a spectrum of mental health conditions. Oxytocin is an evolutionarily conserved hormone and signaling molecule that has emerged as a possible mediator of social deficits and is known to interact intricately with other ancient circuits such as the dopaminergic and serotonergic systems, in ways that remain poorly understood. This project will bring together novel genetic disease models of ADHD and depression with state-of-the-art imaging techniques to delineate how disease-relevant changes in dopaminergic and serotonergic signaling affect oxytocin function and influence social behaviors and drug responses. With these efforts, we seek to uncover new insights into the neural processes of social deficits, with potential implications for developing circuit-based strategies to treat social impairments.

Verena Untiet

Epilepsy affects over 6 million people in Europe and current treatments are mainly focused on relieving symptoms. In neurons from brain slices of patients with epilepsy, the inhibitory neurotransmitter GABA becomes excitatory. In healthy condition, this inhibition is mainly mediated via chloride (Cl-) influx into neurons, which hyperpolarizes the cell and suppresses excitation. The direction of Cl- movement depends on the Cl- gradient across the membrane. Astrocytes are cells in the brain that help maintain ion balance, and I have recently shown that astrocytic Cl- levels can affect how long neurons remain active. My hypothesis is that when Cl- levels are disturbed in astrocytes, neuronal signaling is disrupted. Regulation of Cl- levels in astrocytes might represent a new therapeutic target for treatment of epilepsy. The main goal of the research work is to identify astrocytic Cl- homeostatic pathways as targets for therapeutical strategies to treat epileptic seizures.

Elena Zavala

DNA analyses have transformed the study of our evolutionary past as well as forensic investigations. These application areas, while seemingly disparate, have many similarities. Both use low-quality, degraded DNA to reconstruct past events and are often limited to where skeletal remains were recovered. I wish to develop new methods to use sediment DNA to comprehensively explore human presence at recent and distant timescales. Using sediment DNA from Bronze Age England, I will examine the genetic ancestry and phenotypic traits of people as well as their animal husbandry and domestication practices. I will also investigate how sediment DNA can aid forensic casework by assessing its reliability for the identification of missing individuals. The goals are to study the demographic history of Bronze Age England, aid in forensics investigations, and establish new benchmarks to advance research in both fields.

Stine Helene Falsig Pedersen

Henrik Dimke

There is a 10% risk of developing a kidney stone throughout ones lifetime and recurrence rate is high. The high risk of kidney stone disease imposes a significant burden on the healthcare system and emphasizes the need for improved therapy, including a wider range of medications to combat kidney stone formation. High calcium levels in urine lead to kidney stone formation and this risk can be reduced by decreasing calcium excretion into urine. The calcium-sensing receptor (CASR) is critical for regulating calcium transport in the kidney and the formation of kidney stones. I have discovered new evidence on how the CASR in the kidney increases calcium excretion via novel mechanisms. I will therefore investigate the underlying mechanisms of how the CASR regulates calcium transport in the kidney to uncover new pharmacological targets in the treatment of kidney stones.

Kyung Mih Noh

Our research explores chromatin mechanisms in neurodevelopment and brain disorders. Chromatin comprises DNA and histone proteins and regulates gene expression, which has an impact on human health. Key questions guide our work: How do chromatin regulators impact neuronal identity and, contribute to neurodevelopmental disorders? (2) Do chromatin states causatively regulate gene expression and cellular function? (3) How do neuronal chromatin states respond to external stimuli, and is there chromatin memory in the neuronal process? (4) What chromatin mechanisms govern interactions between neurons and other brain cell types in neurodevelopment? Using cutting-edge functional genomics, human brain cell models, and single-cell sequencing, we aim to decode molecular networks, providing essential insights into the molecular basis of neurodevelopment and brain disorders. Our efforts hold the potential to advance drug development and personalized medicine.

Frederic Gachon

The circadian clock orchestrates human physiology, including when we eat and sleep, synchronizing it with the daily changes in our environment and the alteration of day and night. Modern western lifestyles, technology, and shift work disrupt our body clock. This disruption is associated with many diseases including obesity and liver and kidney diseases, but the mechanisms responsible are poorly understood, as well as the causal relationship: is this circadian disruption a cause or a consequence of these diseases? This project aims at deciphering the consequences of the disruption of the circadian clock, with the hypothesis that the associated perturbations of our hormones could play a role in the progression of these diseases. This will potentially define new strategies to diagnose, prevent, and treat metabolic dysfunction associated diseases.

Lisa Frankel

Throughout their lifetime, cells face many types of stress from the environment including pollution, UV radiation, pathogen infection and exposure to various toxins. In the face of stress, our cells must adapt to survive and maintain vital functions. If not properly managed, genetic mistakes accumulate and predispose to disease, including cancer. One mechanism for coping with stress is autophagy. This system is crucial for the removal and recycling of cellular waste in order to maintain cellular and tissue homeostasis. Autophagy is deeply conserved in evolution and enables cellular adaptation and survival in response to stress. Using state-of-the-art methods, my team will investigate completely new aspects of autophagy, including its ability to reprogram our genetic instructions in response to stress. By illuminating this new layer of gene expression control, we will provide fundamental understanding of cancer development and progression, with importance for therapeutic developments.

Yoshiki Narimatsu

Sugars cover surfaces of all living cells and these glycans are essential for many of the biological processes required for human life and our relationship with the microbial world. Glycans, much like DNA and proteins, contain information that needs to be decoded. Information in glycans is “read” by glycan-binding proteins and these direct biological signals and functions. The simple way we currently understand how proteins read glycans does not provide a plausible explanation for the great diversity of functions assigned to glycans. I therefore propose that glycans are read in more complex ways. I have developed a novel technology that enables analysis of such complex glycan motif, and recently I obtained the first experimental evidence to support my hypothesis. In this project, I will therefore explore how complex glycan motifs modulate our immune system and how bacteria and virus gain entry and cause pathologies through glycans. The project has wide biomedical perspectives.