Dr Bjorn Vahsen

Biography

I studied Medicine and completed my medical doctorate at the University of Göttingen, before undertaking an MSc/DPhil in Clinical Neurosciences and postdoctoral work at the University of Oxford. In 2024, I was a Visiting Research Fellow at Memorial Sloan Kettering Cancer Center in New York. In 2026, I was awarded an independent fellowship from the MND Association and appointed SSIG Lecturer in Neuroimmunology at the University of Aberdeen to start my research group at the IMS.

Prizes and Awards

BNA Postgraduate Prize (2023)

Felgenhauer Research Award of the German Neurological Society (2023)

Junior Research Prize of the German Society for Muscular Diseases (2025)

ENCALS Young Investigator Award Gold Medal (2025)

FTD UK Stuart Pickering-Brown Basic Science Prize (2026)

Research Overview

Our research

We study the cellular and molecular mechanisms of neurodegeneration. We are particularly interested in the role of microglia in major neurodegenerative diseases. Our main focus is on amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two closely related diseases with overlapping clinical phenotype, genetics, and pathology.

We combine human patient-derived iPSC models of increasing cellular complexity with ‘omics and high-throughput imaging approaches to:

1. Understand how genetic ALS/FTD variants impact on microglial biology,

2. Dissect the mechanisms by which microglia drive neurodegeneration in ALS/FTD,

3. Translate this fundamental mechanistic knowledge into novel therapies.

Current projects

Microglia in C9orf72-ALS/FTD

Hexanucleotide repeat expansions (HRE) in C9orf72 are the most common genetic cause of both ALS and FTD. Notably, C9orf72 expression is particularly high in microglia, suggesting a key role for C9orf72 in microglial function. We have previously demonstrated that human iPSC microglia carrying the C9orf72HRE upregulate pro-inflammatory pathways and reduce the survival of motor neurons via dysregulated MMP-9 release (Vahsen et al., 2023). We are now investigating in greater detail how the C9orf72 HRE impacts microglial biology and the specific mechanisms underlying non-cell-autonomous neurotoxicity.

Microglia and TDP-43

Mislocalisation and aggregation of TDP-43 are defining features of ALS and many cases of FTD. Variants in TARDBP (which encodes TDP-43) are also a frequent cause of ALS/FTD. However, the impact of TDP-43 dysfunction on microglial biology remains poorly understood. Using complementary approaches, we investigate inflammatory changes in TARDBP mutant microglia and the interplay between neuronal TDP-43 proteinopathy and microglia.

Advanced neuro-immune models for ALS/FTD

Microglial function is strongly shaped by the cellular environment, including interactions with other neuronal and non-neuronal cell types. We have developed and characterised the first protocol for iPSC-derived motor neuron-microglia co-cultures (Vahsen et al., 2022). We are now developing increasingly complex iPSC-derived model systems to study how microglia interact with and influence other cell types, and how these interactions in turn shape microglial function. These models will provide us with a more refined understanding of neuro–immune interactions in health and disease.

For more details, please check out our lab website.