Eva Hedlund

After receiving her PhD from the Karolinska Institutet, Sweden, Dr Hedlund conducted postdoctoral research both at UCLA School of Medicine -working on spinal cord and motor neuron development and identification of downstream targets of Hox genes - and subsequently at Harvard Medical School - focusing on stem cell therapies for neurodegenerative diseases and later on elucidating disease mechanism in ALS as an ALS Association young investigator awardee. She returned to Sweden and established her own laboratory focused on ALS research at Karolinska Institutet in 2012. In 2020 she was recruited to Stockholm University and moved her laboratory to the Department of Biochemistry and Biophysics while maintaining an affiliation with the Karolinska Institutet.

Research focus of Hedlund lab: Research in my laboratory is aimed at elucidating mechanisms of neuronal vulnerability and resistance with the goal of identifying new molecular targets for the treatment of neurodegenerative diseases, with a particular emphasis on amyotrophic lateral sclerosis (ALS). We are particularly interested in understanding how different neurons modulate their epigenome, transcriptome, and proteome in response to disease-inducing mutations that will lead to the demise of some neurons while others will remain apparently unharmed and how RNAs/proteins are redistributed in somas and axons with disease. In our work we use a wide range of techniques including genome editing of induced pluripotent stem cells using CRISPR/Cas9, in vitro organoid and assembloid formation, microfluidics, single cell RNA sequencing (scRNAseq), single nuclei RNA seq (snRNAseq), proteomics, and gene therapy.

Recent breakthroughs in the Hedlund laboratory include

1. development of the spatial transcriptomics method LCM-seq, which enables scRNAseq of single cells from partially degraded human tissues;
2. identification of IGF-2 as a factor restricted to resilient oculomotor neuron which could prolong the life span of ALS mice after gene therapy;
3. the directed generation of oculomotor neurons from stem cells and demonstration of their relative resilience in vitro;
4. identification of synaptotagmin 13 as a factor in resilient motor neurons and demonstration that overexpression increases lifespan of ALS and spinal muscular atrophy mice significantly;
5. development of Axon-seq for sequencing of neuronal processes;
6. demonstration that a myokine (Neurturin) can switch motor neuron identity from fast to slow through retrograde signaling from muscle.