James Tribble

James Tribble

Assistant Professor
Visiting address: Eye Center of Excellence Avd Ögon & Syn, Eugeniavägen 12, 17164 Solna
Postal address: K8 Klinisk neurovetenskap, K8 Ögon och Syn Williams, 171 77 Stockholm
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About me

  • My research investigates the interaction of neurons, glia, and the vasculature in neurodegeneration, focusing on metabolism and inflammation. We use microscopy, molecular, and multi-omics tools. James received his BSc (Hons) in Medical Pharmacology and PhD in Visual Neuroscience and Molecular Biology from Cardiff University, Wales before undertaking his initial postdoctoral training in the lab of Prof. James Morgan at the School of Optometry and Vision Sciences, Cardiff University where his work has focused on early dendrite and synapse refinement during glaucoma using human patient and glaucoma animal model tissues. James joined the Pete Williams Lab in 2018 to further his postdoctoral education where his work focused on the early mechanisms of neurodegeneration in glaucoma, focusing on mitochondrial and neuronal metabolism. In Nov 2021 James was promoted to Assistant Professor within the Williams Glaucoma Group. 2016 PhD in Visual Neuroscience and Molecular Biology, Cardiff University, UK 2011 B.Sc Medical Pharmacology (hons), Cardiff University, UK

Research

  • My research is focused on the interaction of inflammation and metabolism in the retinal neuro-vascular unit, and how this contributes to neurodegenerative disease. The eye is an ideal model to explore these interactions since it has well defined neuronal layers and vascular plexuses. Glaucoma, one of the most common sight threatening diseases, cause the death of retinal ganglion cells which carry visual information to the brain. My research seeks to understand early mechanisms of disruption to the retinal ganglion cell neuro-vascular unit including resolving metabolic and neuroinflammatory changes. We use high resolution imaging, gene and protein assays, and metabolomic and transcriptomics tools. By understanding these early mechanisms we can identify novel targets for the development of new therapeutics that could help to prevent or slow vision loss.

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