Research groups
Elena Britti
Postdoctoral neuronal cell biologist
After completing my undergraduate and master’s degrees in Biology at the University of Calabria (Italy), I moved to Prof J. Ros’s laboratory (University of Lleida, Spain) with an Erasmus+ (bet for job) fellowship, where I continued as PhD student. There, my research focused on mitochondria and calcium in Friedreich Ataxia (FA), a rare neurodegenerative disease, studying dorsal root ganglion (DRG) sensory neurons. My work demonstrated mitochondrial calcium efflux alteration and mitochondrial dysfunction in frataxin-deficient DRGs and gave some clues about the treatments that could be considered in the future. During my PhD, I was awarded a 3 months-EMBO short-term fellowship as a PhD visiting student in Prof A. Y. Abramov’s laboratory (University College of London, UK), where I was introduced to the roles of mitochondrial calcium in Frontotemporal Dementia (FTD) and Parkinson’s Disease (PD), studying the role of TauK18, a fragment of Tau protein, in cortical neurons and the interaction ER-mitochondria in PD-patients iPSC-derived neurons.
I am currently a postdoctoral neuronal cell biologist in Prof R. Wade-Martins' s laboratory. My research at the University of Oxford focuses on targeting mitochondrial biology in Parkinson’s disease (PD). The aim of this project is to study the role of ubiquitin in the pathogenesis of PD and to develop novel therapeutic approaches using patient iPSC-derived neurons, working with the Oxford Drug Discovery Institute and Bristol Myers Squibb (BMS). In particular, my principal duties are to study the mechanisms of action of modulators of the ubiquitination pathway on mitochondrial biology in cellular models of PD; to develop new scientific (cellular and molecular) techniques to assay the ubiquitination system and mitochondrial biology in iPSC-derived neurons from patients or cell lines and use them for drug screening. The funds supporting this research project are provided by BMS.
Recent publications
Correction: Mitochondrial impairment, decreased Sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich ataxia models.
Journal article
Sanz-Alcázar A. et al, (2025), Cell Mol Life Sci, 82
USP30 inhibition improves mitochondrial health through both PINK1-dependent and independent mechanisms
Preprint
Williamson MG. et al, (2025)
Mitochondrial impairment, decreased sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich Ataxia models.
Journal article
Sanz-Alcázar A. et al, (2023), Cell Mol Life Sci, 81
Mitochondrial iron and calcium homeostasis in Friedreich ataxia.
Journal article
Tamarit J. et al, (2021), IUBMB Life, 73, 543 - 553
Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia.
Journal article
Britti E. et al, (2021), Biochem J, 478, 1 - 20

