Serena Stanga graduated in Chemical and Pharmaceutical Biotechnology (2005) and Pharmaceutical and Medical Biotechnology (2007) at the Univ. of Pavia. There, she obtained the Ph.D. in Pharmacological Sciences with a thesis on Alzheimer’s disease (2010).
From 2011 to 2018 she was Research Associate at the Institute of Neuroscience, Univ. catholique de Bruxelles in Pr. Kienlen-Campard lab. For her research on neuromuscular diseases she was awarded with the Prix Lagast by the Health sector of UCLouvain, Cliniques universitaires Saint-Luc and CHU UCL Namur in 2018. In the same year, she earned a Master in Translational Medicine at the Univ. libre de Bruxelles.
In fall 2018 she joined Prof. Vercelli’s group at the Neuroscience Institute Cavalieri Ottolenghi as Researcher and in 10/2021 she became Assistant Professor (RTD-B) in Human Anatomy Dep. of Neuroscience, Univ. of Torino. Since November 2023 she is member of the Scientific Board of the Ph.D. School in Neuroscience and since October 2024 she is Associate Professor in Human Anatomy Dep. of Neuroscience, Univ. of Torino.
Research focus
Serena Stanga is interested in understanding the molecular mechanisms underpinning neurodegeneration to find new potential biomarkers for early diagnosis and therapeutic targets to open new roads toward delaying or eliminating the onset of many age-related diseases, such as dementia and motor neuron diseases. In this regard, she believes that understanding brain aging is essential to the pursuit of brain health.
By means of different in vitro and in vivo models, biochemical and histological analysis, advanced imaging and live approaches, she focuses on the study of mitochondria morphology and function, brain iron metabolism and neurotrophic growth factors’ alterations in AD and ALS. In her scientific track record, she showed that those events represent early phenomena associated with aging, amyloid deposition, neuron and motor neurons’ degeneration.
Currently, she is trying to depict how these phenomena interact and affect each other causing the onset/progression of neurodegeneration.
