Prof. Sivan Henis-Korenblit is a Senior Lecturer in the Mina and Everard Goodman Faculty of Life Sciences. She came to Bar-Ilan University from the University of California, San Francisco, as part of the 2009 cohort of returning scientists, a special program within Bar-Ilan University to recruit young Israeli scientists to return to work in Israel.
Henis-Korenblit’s main research interest is in identifying the molecular mechanisms of aging using the model organism C. elegans. In particular, her lab focuses on the link between aging, age-related disease and protein quality control. Henis-Korenblit’s research has specific applications in a variety of maladies such as cancer, diabetes and neurodegenerative diseases such as Alzheimer’s disease, all of which are closely associated with age.
Human aging is accompanied by an overall decline in physiological function and an increase in the incidence of age-related diseases. It is now clear that aging is a highly conserved and regulated process. Researchers at Henis-Korenblit’s lab believe that a greater understanding of the genetic and molecular mechanisms underlying the aging process will ultimately lead to the ability to reduce and delay aging, along with the symptoms and diseases associated with it.
Henis-Korenblit and her team use the round-worm C. elegans to explore which genes and pathways control the rate of aging. At the molecular level, C. elegans and humans share the same universal mechanisms of life. By editing the genetic code, Henis-Korenblit and her researchers make use of this model organism to identify conserved genes and pathways that slow down aging. This is the first step towards understanding how to actively gain control over the rate of aging.
Age is a major risk factor in our susceptibility to a variety of neuro-degenerative diseases such as Alzheimer’s, Huntington’s and Parkinson’s disease. Henis-Korenblit and her team explore how genes related to aging affect the body’s tendency to succumb to neurodegenerative conditions. Working with C. elegans models of these diseases, they hope to clarify whether genes and pathways that control the rate of aging can postpone or even cure these neurodegenerative disorders, paving the way toward novel therapeutic approaches.
Many of these neurodegenerative diseases are associated with the accumulation of misfolded proteins that may contribute to the deterioration of cells, and hence to the deterioration of tissues and the whole body. Thus, Henis-Korenblit and her researchers also study how genetic manipulations that improve protein folding and protein quality affect these age-related disease models. In particular, the lab is interested in pathways that concomitantly improve protein quality and slow down aging, as these may provide an optimal cellular setting to combat age-related diseases. One such pathway that is studied extensively in the lab is the insulin/IGF-1 pathway. Henis-Korenblit and her group also investigate how pathways that control aging and pathways that control protein folding interact and impact each other.
Knowledge gained in Henis-Korenblit’s lab about the conserved molecular genetics underlying cellular and organism aging in C. elegans can potentially be applicable to humans. In the long term, their aim is to develop tools to improve the quality of life of older individuals, and to delay and prevent age-related disease.