Dr. Elsa Logarinho

i3S- Instituto de Investigação e Inovação em Saúde

E. Logarinho concluded her PhD in Biomedical Sciences by the University of Porto (UP) in 2002. After her PhD, E. Logarinho embraced a teaching position at the ISCS-N/CESPU Health Sciences School, while maintaining her research affiliation at IBMC. In 2007, E. Logarinho joined the Medical School/ICVS/UMinho as full-time Assistant Professor, and pursued her research in Cell cycle/Mitosis, as well as contributed to several publications in other scientific areas.
In 2009, E. Logarinho returned to full-time research career path under Ciência 2008 program. Her work at IBMC on mechanisms ensuring mitotic spindle-pole integrity (Nat Cell Biol 2012) was acknowledged with the Pfizer 2011 and SPGH 2013 prestigious national prizes.
In July 2013, she was awarded a Junior Researcher position to launch innovative research lines at IBMC (now part of the i3S Consortium/UP). Following a 2-year period, she established her research group Aging & Aneuploidy, and simultaneously was awarded with a 5-year FCT Assistant Researcher position. Currently, her research group is composed of 3 Post-Docs and 4 PhD students, working on to decipher mechanisms of mitotic dysfunction and aneuploidy contributing to aging and age-related diseases. Using trisomic amniocytes, she demonstrated that aneuploidy per se induces chromosomal instability, generating genetic heterogeneity (Elife 2015), which in turn provides selective advantage under stressful conditions typically found in tumour microenvironment (Sci Rep 2016). Using elderly dermal fibroblasts, she proved that aneuploidy increases with aging due to general dysfunction of the mitotic machinery, which correlates with an early senescence-associated signature and repression of the FoxM1 transcription factor of late cell cycle gene cluster. By restoring FoxM1 levels in elderly and progeria fibroblasts, aneuploidy was prevented and cellular aging phenotypes rescued (Nat Commun 2018). These studies provided the basis for her current and future research on addressing the impact of mitotic competence rewire in the improvement of aging hallmarks and as an anti-aging strategy, further using mouse models.