Bio

Themis completed his PhD at the Centre for Discovery Brain Sciences of the University of Edinburgh in Scotland under Prof Catherina Becker, with focus on the contribution of the innate immune system during regeneration of the zebrafish spinal cord. As a postdoctoral researcher with Prof Anna Williams at the Centre for Regenerative Medicine in Edinburgh he worked on the molecular mechanisms that regulate the differentiation and functional maturation of human oligodendrocytes. Over the last few years, he worked on several projects focused on the identification of genes that regulate the axonal regeneration of spinal cord after injury and the differentiation of human oligodendrocyte progenitor cells into myelin producing oligodendrocytes. As a member in the Gibson lab, Themis aims to identify molecular regulators of the circadian clock and how tuning the circadian system affects the maturation and function of oligodendrocytes in health and disease.

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All Publications

  • Protocol for assessing myelination by human iPSC-derived oligodendrocytes in Shiverer mouse ex vivo brain slice cultures. STAR protocols Tsarouchas, T. M., Zoupi, L., Williams, A., Gibson, E. M. 2025; 6 (1): 103609

    Abstract

    Human induced pluripotent stem cell (iPSC)-derived oligodendrocytes are a powerful tool for studying aberrant myelination in neurodegenerative and neurodevelopmental disorders; however, they often fail to myelinate in vitro. Here, we present a protocol for axonal ensheathment and perinodal segmentation using an ex vivo model. We describe steps for preparing Shiverer mouse brain slice cultures, oligodendrocyte transplantation, visualization, and analysis. This approach suits multiple culture formats, highlighting the potential for the screening of myelin-modulating drugs and compounds in a cost- and time-effective manner, while reducing animal use.

    View details for DOI 10.1016/j.xpro.2025.103609

    View details for PubMedID 39888721

  • C9ORF72 deficiency results in neurodegeneration in the zebrafish retina. The Journal of neuroscience : the official journal of the Society for Neuroscience Jaroszynska, N., Salzinger, A., Tsarouchas, T. M., Becker, C. G., Becker, T., Lyons, D. A., MacDonald, R. B., Keatinge, M. 2024

    Abstract

    Hexanucleotide repeat expansions within the gene C9ORF72 are the most common cause of the neurodegenerative diseases Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal dementia (FTD). This disease-causing expansion leads to a reduction in C9ORF72 expression levels in patients, suggesting loss of C9ORF72 function could contribute to disease. To further understand the consequences of C9ORF72 deficiency in vivo, we generated a c9orf72 mutant zebrafish line. Analysis of the adult female spinal cords revealed no appreciable neurodegenerative pathology such as loss of motor neurons, or increased levels of neuroinflammation. However, detailed examination of adult female c9orf72-/- retinas showed prominent neurodegenerative features, including a decrease in retinal thickness, gliosis, and an overall reduction in neurons of all subtypes. Analysis of rod and cone cells within the photoreceptor layer showed a disturbance in their outer segment structure and rhodopsin mis-localisation from rod outer segments to their cell bodies and synaptic terminals. Thus, C9ORF72 may play a previously unappreciated role in retinal homeostasis and suggests C9ORF72 deficiency can induce tissue specific neuronal loss.Significance statement Hexanucleotide expansions in the gene C9ORF72 are the most common cause of the Amyotrophic lateral sclerosis (ALS)/ Frontotemporal dementia (FTD) disease spectrum. The expansion reduces expression of C9ORF72 and so may play a role in neuronal loss. However, C9ORF72 loss of function has been comparatively understudied in vivo. Using the zebrafish as a model of C9ORF72 deficiency, we demonstrate that loss of C9ORF72 results in marked inflammation and neuronal loss in the aged adult zebrafish retina. Development of the retina is unaffected regardless of C9ORF72 status. This demonstrates that C9ORF72 loss of function can cause spontaneous neurodegeneration in vivo and highlights a novel role of C9ORF72 in retinal homeostasis.

    View details for DOI 10.1523/JNEUROSCI.2128-23.2024

    View details for PubMedID 38658168