Dr. Diana Jurk, Ph.D. is an Associated Professor at Mayo Clinic Rochester and directs the Biology of Aging and Age-related Diseases laboratory.
Dr. Jurk is originally from Germany where she graduated with a degree in Natural Sciences from the University of Freiberg in 2004. Following her degree, she conducted biomedical research at Bayer, first in Wuppertal and then in Leverkusen (where she was awarded a master's degree).
Having decided to move to academia, Dr. Jurk was first a research assistant at the Uniklinik in Freiburg, Germany (2005-2007) and then conducted her PhD studies at Newcastle University in the UK (2007-2012), in the area of liver senescence and inflammation.
In 2015, Dr. Jurk was awarded the Newcastle University Faculty fellowship and in 2018 the prestigious Springboard Award from The Academy of Medical Sciences which allowed her to direct an independent research program. In 2018 she moved her research team to Mayo Clinic, Rochester.
Diana's work has led to new insights into the mechanisms driving the process of cellular senescence in the context of liver disease and neurodegeneration. Her work, published in Nature Communications, has demonstrated a key role for senescence in Non-alcoholic fatty liver disease. More recently, her team published in Cell Metabolism the first evidence for the involvement of senescence in neuropsychiatric diseases and in cognitive decline during aging (Aging Cell, 2021).
Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown to improve brain function in mouse models of neurodegenerative diseases as well as obesity. However, it is still unknown whether senescent cell clearance alleviates cognitive dysfunction during the aging process. To investigate this, we first conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice. We observed an age-dependent increase in p16Ink4a senescent cells, which was more pronounced in microglia and oligodendrocyte progenitor cells and characterized by a SASP. We then aged INK-ATTAC mice, in which p16Ink4a-positive senescent cells can be genetically eliminated upon treatment with the drug AP20187 and treated them either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin. We observed that both strategies resulted in a decrease in p16Ink4a exclusively in the microglial population, resulting in reduced microglial activation and reduced expression of SASP factors. Importantly, both approaches significantly improved cognitive function in aged mice. Our data provide proof-of-concept for senolytic interventions' being a potential therapeutic avenue for alleviating age-associated cognitive impairment.
