Ana Domingos
Associate Professor of Neuroscience
Tell us a bit about your role
I’m a scientist. I got to where I am now by pursuing the answers to the questions that I’m interested in: questions relating to the organization and function of living systems and cells. Namely, questions relating to the cross-talk between neural circuits, immune cells and adipocytes.
To this end, I’ve trained and worked at many different institutions, moving from one country to another. The experience of being exposed to different environments makes you think out-of-the-box. That diversity of experience is fertile ground for innovation in research. After studying Mathematics MSc in my home county of Portugal and also in Paris, I did my PhD at The Rockerfeller University in New York City studying the neurobiology of olfactory systems in fruit flies. I stayed there for my postdoc under Jeffrey Friedman investigating how the hormone leptin affects neurocircuitry underlying food choices in mouse models of obesity. I further pursued research into neuroimmune mechanisms underlying obesity by starting my first lab in my home country before successfully applying for an Associate Professor role at the Department of Physiology, Anatomy and Genetics (DPAG). Here, my role as a scientist devoted to the search for answers to untapped questions within life sciences fits the wider landscape of the Medical Sciences at Oxford University.
What is the most meaningful aspect of your work?
Discovery in itself is the most meaningful aspect of my work – to me. To patients it may be the hope of cure: I receive lots of supportive emails from obese patients whenever I publish a paper congratulating me on dedicating my life to studying their condition. While I don’t run clinical trials, they often want to volunteer themselves as patients.
Can you tell us about something you've done or contributed to that you're most proud of?
I’m proud that my laboratory discovered the sympathetic neuro-adipose junction, a functional synapse-like connection between white adipocytes and the sympathetic nervous system (published in Cell, 2015). We found that this neuro-adipose junction is necessary and sufficient for fat mass reduction via norepinephrine (NE) signaling (Cell, 2015 and Nature Communications, 2017). We then discovered Sympathetic neuron-Associated Macrophages (SAMs) that directly import and metabolize NE. Abrogation of SAM function promotes long-term amelioration of obesity independently of food intake (Nature Medicine, 2017). These findings inspired the development of a new class of anti-obesity compounds named sympathofacilitators, which do not enter the brain, nor have the typical cardiovascular side effects of centrally acting sympathomimetic drugs (Cell Metabolism, 2020). Sympathofacilitator drugs act as an energy sink by coupling thermogenesis to active heat dissipation.
What changes would you most like to see in the medical sciences in the next 100 years?
I would like to see paradigm-shifting discoveries that accelerate biomedical research for the greater good of humanity and the planet.