SUMMARY
Diana Jurk, Ph.D., investigates the mechanisms leading to aging and age-related diseases and has made important contributions to the fields of liver disease and neurodegeneration.
In the field of liver disease, Dr. Jurk demonstrated that inflammation is a key driver of cellular senescence in hepatocytes, contributing to impaired regenerative capacity, fibrosis and cancer. Additionally, Dr. Jurk was the first to demonstrate that clearance of senescent cells in aged, obese or diabetic mice can alleviate hepatic steatosis, suggesting that elimination of senescent cells can be a novel therapeutic strategy against nonalcoholic fatty liver disease.
In the field of neurodegeneration, Dr. Jurk was the first to identify that during aging, post-mitotic neurons acquire a senescent-like phenotype, a phenomenon driven by telomere dysfunction. As part of her independent research program, Dr. Jurk investigated further the role of cellular senescence in the brain in the context of obesity. Her team was the first to demonstrate that senescent cells inhibit neurogenesis, contributing to obesity-induced anxiety-like behavior. This led to the novel concept that senolytic drugs are a potential new therapeutic avenue for treating neuropsychiatric disorders, such as anxiety and depression.
Focus areas
- The role of senescence in brain aging and neurodegenerative diseases. Age is the single most relevant factor for developing neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, that contribute to significant cognitive decline. Dr. Jurk's team has demonstrated that cellular senescence occurs during brain aging; however, it is still unknown how senescence affects brain function. Dr. Jurk's research program aims to understand and identify novel molecular mechanisms contributing to senescence during age-related neurodegeneration and to identify new therapeutic targets.
- Senescent cells in obesity. Dr. Jurk's research has shown that senescent cells play a pivotal role in obesity-induced anxiety-like behavior. Additionally, she has discovered that senescent cells are less effective in lipid metabolism, resulting in the unwanted accumulation of fat depots. The team is currently investigating the consequences of fat accumulation in senescent cells as well as the molecular mechanisms contributing to impaired lipid metabolism in these cells, aiming to identify novel targets for interventions to counteract senescence in the brain.
- Inflammation, senescence and neurodegeneration. Most neurodegenerative diseases are characterized by chronic inflammation; however, the mechanisms involved are still not completely understood. A major goal of Dr. Jurk's research is to identify the relative contribution of senescence of different cell types and regions in the brain to neuroinflammation. Understanding the relationship between cellular senescence and neuroinflammation could suggest novel strategies for treatment of neurodegenerative diseases.
Significance to patient care
Dr. Jurk's research aims to find new ways to prevent or delay the onset of age-related diseases and thereby extend healthy lifespan. Aging is a complex phenotype characterized by multimorbidities. Dr. Jurk aims to understand the basic mechanisms driving the aging process with the ultimate purpose of targeting not one but multiple age-related diseases simultaneously.