We work on rare diseases, too

Celebrating Rare Disease Day with our colleagues at the BioISI research unit, at the Faculty of Sciences, University of Lisbon.

More on rare disorders in our research unit: https://bioisi.pt/biorscide-science-days-and-ephemeris-rare-disease-day/


My scientific background is cellular and molecular biology of the central nervous system in normal and pathological conditions, with especial focus on neurodegeneration and neuroprotection. My PhD thesis (University of Oviedo, Spain) focused on the intracellular mechanisms underlying the neuroprotective and antitumoral effects of melatonin and other indoleamines, which could be used as starting reference molecules for the development of drugs against neurodegenerative disorders or brain cancer. As a postdoctoral fellow at the Salk Institute (La Jolla, CA, USA), I studied neural precursor cell differentiation. My findings could be relevant for the understanding of Down´s syndrome and the success of regenerative medicine in CNS pathologies involving cell loss, such as spinal cord injury or neurodegenerative disorders. As a postdoctoral fellow at the Instituto de Medicina Molecular (Lisbon, Portugal), I identified genes and small molecules that prevent aberrant protein-protein interactions in the context of neurodegenerative disorders, by means of bimolecular fluorescence complementation (BiFC) assays we developed in-house. In 2014, I established my own laboratory at the Instituto de Tecnologia Quimica e Biologica (Oeiras, Portugal), with two major goals: 1) unravel the intracellular pathways involved in neural precursor cell differentiation and 2) develop new optogenetic tools for the control of cell behavior and fate. I am currently a professor and laboratory head at the Faculty of Sciences, University of Lisbon, where we continue to explore these issues with special focus on the JAK/STAT3 pathway. However, we have growing interest in the role of glial cells on rare neurological disorders, such as Alexander´s or Huntington´s diseases, ARSACS or NKX6-2-related ataxia.