In 2025, DANDRITE strengthened its role as a hub for curiosity‑driven, interdisciplinary neuroscience, uniting molecular mechanisms with systems‑level perspectives on brain function and disease.
As the Danish node of the Nordic EMBL Partnership for Molecular Medicine, we continued to combine international excellence with a dynamic and expanding research environment at Aarhus University.
This year, our group leaders advanced ambitious scientific programs that broadened DANDRITE’s scope—from uncovering regulatory principles in brain cell states to developing transformative technologies for tracing cellular history and probing synaptic function.
2025 brought significant conceptual and technological breakthroughs, accompanied by strong team growth and diversified funding. Together, our researchers are building the foundations for long‑term impact: generating fundamental insights, developing new tools, and training the next generation of neuroscientists. These efforts reflect DANDRITE’s core vision—to bridge molecular and cellular discoveries with translational opportunities, ultimately contributing to new strategies for understanding, diagnosing, and treating brain disorders.
The group opened in August 2025. In the remaining year, we successfully secured and built-up research infrastructure. We performed the first dual patch-clamp recordings in acute slices of adult mouse thalamus. Our ERC starting grant 2025 was successfully transferred to Aarhus in December 2025.
We overcame many foreseen and unforeseen challenges associated with starting a new group in a new country. Challenges included, but were not limited to, countryspecific research and funding organization, delayed allocation of lab space, and completing the move of DANDRITE labs across campus.
We look forward to start building our experimental setups in the lab space provided from March 2026. While we finish building the infrastructure, we will recruit motivated and talented group members to dive together into experiments exploring thalamic visual circuits
In 2025, our group identified peripheral inflammatory signatures associated with negative affect during acute sickness and the subsequent recovery phase. Using high-dimensional proteomics, we observed coordinated immune signaling related to immune-cell activation, migration, and barrier communication during sickness, while anti-inflammatory signaling remained elevated during recovery.
In collaboration with Boris Heifets at Stanford University, we also identified characteristic neural and microglial activity patterns linked to acute sickness and affective recovery. Together, these findings provide new insight into immune-to-brain communication and may help explain inconsistencies across previous clinical studies of affective state during inflammation.
In parallel, we continued developing chemogenetic strategies to manipulate microglial states in our Parkinson's disease models. Preliminary findings suggest that modulating specific microglial states can restore aspects of healthy behavior in disease-model mice. These studies contribute to a broader understanding of neuroimmune signaling in both neurodegeneration and affective state regulation, while opening new avenues for selectively targeting microglial function in disease.
A major challenge during 2025 has been the implementation and validation of activity-dependent targeting strategies combined with glial manipulations and optogenetic approaches. While early results are promising, additional validation is needed to confirm the specificity of the methods.
We have also encountered limitations in some inhibitory manipulation strategies targeting the Lateral Septum in vivo. Discussions with international collaborators suggest that these challenges are not unique to our laboratory, and we are therefore evaluating alternative technical approaches moving forward.
In 2026, we aim to further characterize the microglial states induced by our chemogenetic manipulations and define their molecular and functional profiles in greater detail. We also aim to complete a comprehensive characterization of the internal and external connectivity of the Lateral Septum involved in inflammatory models.
More broadly, our goal is to continue integrating immunology, systems neuroscience, and behavior to better understand how immune signaling shapes brain function in health and disease.
This year, the group established STAT1 as both required and sufficient for lipid droplet accumulation in inflammatory microglia, defining a regulatory entry point into a lipid-handling state relevant to Alzheimer's disease. In-house single-cell transcriptomic and epigenomic datasets across AD models, knockouts, and brain regions now anchor the lab's two main directions: microglial state regulation and neuronal vulnerability. Funding diversified with two DFF Project 1 grants, two NORPOD postdocs, and a Parkinsonforeningen pilot, and the team grew to three postdocs, two PhD students, plus master's, bachelor's, and technician roles.
The lab's flagship manuscripts did not reach submission within 2025 and are now scheduled for H1 2026. Personnel turnover and Lab relocation required rebuilding operational capacity in parallel with onboarding the autumn 2025 cohort.
Submit the lab's first independent manuscripts: the state-constraints review, STAT1 lipid droplets, cortical neuronal vulnerability, and the methods paper. Move from programme discovery to predictive modelling of neuronal vulnerability and to metabolic capacity as a control variable in microglial state transitions. Recruit a computational postdoc to bring predictive modelling in-house.
This year, our group made advances in developing new tools for studying the synapse. For example, we developed a specialized deep learning model for predicting protein localization at neuronal synapses. This tool is now routinely used in our lab to uncover new biology at synapses. In addition, we have also built a multidisciplinary toolbox for studying protein damage and clearance at synapses, a fundamental mechanism for modifying synapses during learning. Our efforts directly support DANDRITE’s goal to uncover opportunities for molecular medicine in the nervous system.
Our key challenge in 2025 was to integrate large sets of data obtained from multidisciplinary experiment paradigms as well as to secure funding for the next 4-5 years, which will allow us to sustain a multidisciplinary team. We are still working on analyzing and understanding these datasets now.
In 2026, we aim to elucidate how cellular signals for protein quality control regulate synapses. As the team joins efforts in many datadriven investigations, we hope to obtain novel insight into molecular mechanisms that protect synapses from dysfunction.
In 2025, our group reached a major milestone by posting our first independent lastauthor preprint on HisTrac-seq, a molecular recording technology that enables wholegenome, single-cell, multimodal history tracing in the brain. This work establishes a new framework for moving beyond snapshot-based genomics and retrospectively linking past regulatory states with present cellular identity and function.
A major challenge in 2025 was transforming very challenging technologydevelopment project into a mature and coherent study. This required the integration of molecular biology, viral delivery, single-cell chromatin profiling, large-scale sequencing, and computational analysis. Through this process, the team became more independent, and our experimental and analytical workflows became substantially more robust.
In 2026, our goal is to submit another major preprint on single-cell multiomic analysis of engram cells, the cellular substrate of memory in the brain. By combining this work with the HisTrac-seq preprint, we aim to establish the lab’s defining direction: using cutting-edge genomics and molecular recording technologies to uncover the molecular mechanisms of memory formation.
This year, our group assembled a functional optical trap to move bacteria using light. With this tool we will be able to control the interactions between the fish and bacteria with unprecedented precision. We also have made progress in mapping where inflammation is represented in the brain of zebrafish, which we will follow up with experiments to control inflamma-tion from the brain side, or from the immune side. We have onboarded new team members who have looked at the effects of nanoplastics on the gut of the fish, and we are now following up on these experiments.
The major challenges of 2025 were in managing all the demands of teaching, research, and leading a group. As well as deciding which exciting projects to stop, as there is limited time in a day. A personally rewarding moment was two of my lab members getting a prize at a FEBS conference, and being invited to write a review on immunology in zebrafish.
In 2026, our main goals remain to finalize our manuscripts, and go from proof of concepts to fully fleshed experiments. The team is now up and running, and we have started new collaborations which we are excited to delve into.
