Institute for Cell and Molecular Biosciences

Staff Profile

Dr Diana Jurk

Principal Investigator

Background

Academic degree

  • 2007-2012   PhD at the Faculty of Medical Science, Newcastle University “The role of cell senescence and inflammation in mouse ageing”
  • 1997-2004   Degree in Natural Sciences (Diplom-Naturwissenschaftler) TU Bergakademie Freiberg, Germany

 

Research Experience

  • March 2015 Faculty Fellow in the Institute for Cell & Molecular Biosciences (ICAMB) / Newcastle University Institute for Ageing (NUIA)
  • 2015 Jun-Sep Visiting scientist at Mayo Clinic (Robert and Arlene Kogod Center on Aging) Rochester (MN, US)
  • 2012- 02/2015 Research Associate in the Newcastle University Institute for Ageing (NUIA) / Institute for Cell & Molecular Biosciences (ICAMB)
  • 2007-2012 PhD at Newcastle University (UK)  under the supervision of Professor T von Zglinicki
  • 2009 Visiting scientist at the Max-Planck Institute on Stem Cell Ageing lead by Professor Lenhard Rudolph, Ulm University (Germany) 
  • Feb 2007-Aug 2007 Research Technician at the Centre for Integrated Systems Biology of Ageing and Nutrition (CISBAN), Newcastle University, UK
  • 2005-2007 Research assistant at The Medical Center-University of Freiburg (Germany), Core facility Genomics lead by Dr. Dietmar Pfeifer
  • 1997-2004   3 different work placements of 6 months each at Bayer AG (Wuppertal, Wuppertal-Elberfeld and Leverkusen, Germany)

 

Prizes and awards

  • Travel bursary for 7th Annual Robert and Arlene Kogod Center on Aging Conference, Jacksonville (FL, US) 2016
  • Travel bursary for 5th Annual Robert and Arlene Kogod Center on Aging Conference, Rochester, (MN, US) 2014 awarded by Mayo Clinic (Rochester, MN, US)
  • Travel bursary for Cold Spring Harbor Asia Conference, Suzhou(China) 2013 awarded by IAH (Newcastle University)
  • Travel bursary for 3rd Annual Robert and Arlene Kogod Center on Aging Conference, Rochester, (MN, US) 2012 awarded by Mayo Clinic (Rochester, MN, US)
  • Awarded BSRA bursary for being UK representative at the American Aging Association Meeting in Phoenix, Arizona 2009
  • Awarded best talk prize at the BSRA 2008 Annual scientific Meeting in Brighton (UK)

 

Conferences

Oral Presentations
  • BASL Annual Meeting 2017, Warwick (UK)
  • International Cell Senescence Association (ICSA) Conference 2017, Paris (France)
  • Molecules, Genes and Cells Club, Newcastle University, Newcastle (UK), 2016
  • MIA-Summer School: Biology of Ageing, Alvor (Portugal), 2016
  • 6th Annual Alliance for Healthy Aging Conference, Slaley Hall, Newcastle (UK), 2015
  • CIMA Scientific Meeting, ‘Nutrition and Musculoskeletal Ageing, Newcastle (UK), 2014
  • The Rank Prize Funds, Mini-symposium on Oxidative Stress, Grasmere (UK), 2014
  • Cold Spring Harbor Asia Conference, Suzhou (China) 2013
  • Ageing and Basic Bioscience Conference, Cambridge (UK), 2012
  • Swedish Telomere and Telomerase Network Meeting, Fiskebäckskil (Sweden) 2010
  • Gordon Research Seminar, Les Diablerets (Switzerland), 2010
  • CISBAN Symposium, Newcastle University, 2009
  • 38th Annual Meeting of the American Aging Association, Scottsdale (AZ, US) 2009
  • BSRA, Annual Scientific Meeting, Brighton (UK), 2008

 

Poster Presentations
  • 5th Alliance for Healthy Aging Symposium, Rochester (MN, US), 2014
  • 4th Alliance for Healthy Aging Symposium, Groningen (Netherlands), 2013
  • 3rd Alliance for Healthy Aging Symposium, Rochester (MN, USA) 2012
  • Gordon Research Conference, Ventura (CA, US), 2012
  • BSRA Annual Scientific Meeting, Brighton (UK), 2011
  • Gordon Research Conference, Les Diablerets (Switzerland), 2010 BSRA Annual Scientific Meeting, Newcastle 2010 BSRA Annual Scientific Meeting, Manchester (UK), 2009

Research

 

Cellular Senescence is most often induced as a response to persistent DNA damage and telomere dysfunction, leading to a massive cellular re-programming including hyper-production of reactive oxygen species (ROS) and secretion of bioactive peptides known as the senescence associated secretory phenotype (SASP). It occurs in vivo and contributes to age-related diseases.

As part of my PhD, I have demonstrate that ageing mice neurons show multiple hallmarks of cell senescence. Moreover, I proved that this phenotype can be induced by telomere-dysfunction and is dependent on cyclin-kinase inhibitor p21. This was the first time that a senescent-like state was observed in post-mitotic neurons in vivo and has led to the recent proposal by several reputed researchers of a redefinition of senescence as a phenotype not exclusive to proliferation competent cells. Furthermore, I have shown how cellular senescence induced by genotoxic or oxidative stress depends on chronic DNA-damage signalling from irreparable damage to telomeres. This work showed that telomere-associated DNA damage foci (TAF) existed irrespectively of telomere length and presence of telomerase in a variety of mice tissues and that TAF are a sensitive and robust marker for senescence. More recently, I have demonstrated that nfkb1-/- mice develop chronic systemic inflammation which aggravates cell senescence in various tissues, inducing an accelerated ageing phenotype and decreasing lifespan. This paper establishes a link between chronic inflammation, cellular senescence and ageing.

My current research focuses on senescence during brain ageing and in neurodegenerative diseases like Alzheimer’s and Parkinson’s disease. Age is the single most relevant factor for developing neurodegenerative diseases which contribute to significant cognitive decline. I have demonstrated that cellular senescence occurs during brain ageing. However, it is still unknown how senescence in the brain impacts on its function during ageing. I aim to understand exactly how cellular senescence contributes to brain ageing and age-related cognitive decline. 

Additionally, cellular senescence is a major contributor to age related tissue degeneration and has been shown to be involved in non-alcoholic fatty liver disease (NAFLD), but the mechanisms driving NAFLD are largely unknown. I aim to understand how cellular senescence might contribute to liver disease and if elimination of senescent cells could be used as a therapy to slow down, counteract NAFLD or prevent progression of NAFLD to HCC.

 

 

Teaching

Teaching

In the last 3 years I supervised two undergraduate students, 2 master students and I am supervising three PhD students (Mikolaj Ogrodnik, Edward Fielder, Melanie Weigand).

Publications