Björn Vahsen

I graduated from medical school at the Georg-August-University Göttingen in Germany with both a medical degree and a research MD (summa cum laude and prize for the best thesis of the year). My MD project with Paul Lingor investigated the role of the autophagic protein ULK1 in axonal degeneration and regeneration. I subsequently completed an MSc in Neuroscience and a DPhil in Clinical Neurosciences at the Oxford Motor Neuron Disease Centre with Kevin Talbot and Martin Turner, focusing on the role of microglia in ALS. During my DPhil I was a Clarendon Scholar and held additional scholarships from St John’s College, the MRC, and NIHR. I am now a Postdoctoral Researcher in the Talbot Lab and Junior Research Fellow at Kellogg College, having previously served as Fulford Junior Research Fellow at Somerville College. My work on microglia in ALS has been recognised with the British Neuroscience Association Postgraduate Prize (2023), the German Neurological Society’s Felgenhauer Research Award for Young Neuroscientists (2023), the Junior Research Prize of the German Society for Muscular Diseases (2025), and the ENCALS Young Investigator Award Gold Medal (2025)

For more details, have a listen to this interview with the Cortex Club podcast. 

My research focuses on the role of non-neuronal cells in amyotrophic lateral sclerosis (ALS) pathophysiology and their potential as therapeutic targets. I have a particular interest in microglia (brain immune cells) and their contribution to motor neuron dysfunction and death in ALS. 

I use induced pluripotent stem cell (iPSC) models to derive ALS-relevant cell types (human microglia and motor neurons) from people with genetic forms of ALS to answer two main questions:

1) How do ALS-associated mutations affect microglial biology?

2) Do microglia with ALS-associated mutations affect motor neuron function and what are the underlying mechanisms?

I have developed a co-culture system of iPSC-derived motor neurons and microglia, allowing the investigation of how microglia affect motor neurons in ALS (Scientific Reports, 2022). Using this system, I have shown that microglia with the commonest ALS associated mutation, a hexanucleotide repeat expansion in the C9orf72 gene, are pro-inflammatory and toxic to co-cultured motor neurons. This toxicity was partly mediated by MMP9 (Nature Communications, 2023).  

My work has been funded by the Motor Neurone Disease Association, MND Scotland, a Medical Sciences pump priming grant, an ARUK pump priming award, and a Rosetrees Trust seedcorn grant.