Systems Biology of Ageing and Disease
Ageing is the biggest risk factor for neurodegeneration, cardiovascular disease and cancer. To combat age-related disease we need to understand whether ageing is a biological programme that gets activated as our body matures or an inevitable consequence of wear and tear? The recent discovery that changes to a single gene can increase the lifespan in a variety of animals and the existence of very short-lived vertebrates such as the turquoise killifish, whose average life-span is just six months, seem to suggest that ageing may be partly predefined by a programme written into our DNA.
As humans age, we accumulate increasing numbers of stressed cells, called senescent cells, within our organs. These cells stop dividing and no longer perform their original function; as their number increases, the ability of an organ system to do its job may decrease. Recently a mouse model with severe ageing features, such as muscle loss and cataracts was “cured” through selective killing of senescent cells, suggesting that senescence is one of several cellular ageing mechanisms that contribute to the effects of ageing. We study mechanisms of ageing in a variety of cellular contexts, including cells isolated from older individuals (and even centenarians) and children suffering from premature ageing syndromes. Cells from healthy young individuals stop dividing after a certain number of cell divisions in culture (replicative senescence) or after exposing the cells to certain cellular stresses (oncogenic stimulus and stress-induced senescence).
|Dr Tamir Chandra||Group Leader|
|Nattaphong Rattanavirotkul||PhD Student|
|Daniel Simpson||PhD Student|
|Angela Salzano||Research Fellow|
Ageing, Cellular Senescence, Cancer, Systems Biology, Single Cell Genomics
Hi-C, Single Cell Genomics