Tara Walker

We are interested in understanding the fundamental mechanisms governing the lifelong production of neurons in the adult brain. Adult neurogenesis, as this process is termed, decreases with age and this age-related decline in neurogenesis results in an associated decline in learning processes that are controlled by the hippocampus.

In previous work, together with Professor Perry Bartlett, we provided the first evidence of a true, but normally latent, hippocampal stem cell population and identified a mechanism through which the production of new neurons could be stimulated to replace or repair damaged cells in neurodegenerative diseases. More recently our focus has been on the systemic regulation of adult neurogenesis. We use the physical exercise model of increased neurogenesis to investigate cross-talk between the brain and the peripheral immune system, and in this context have investigated the interaction between T cells, mast cells and platelets and the neural stem cell niche.

The control of cell death provides a key mechanism in the regulation of adult hippocampal neurogenesis. We have demonstrated that ferroptosis, a recently identified, caspase-3-independent mode of programmed cell death, is a fundamental mechanism underlying the regulation of adult hippocampal neurogenesis. This form of cell death is mediated by the dietary trace element selenium. We have shown that selenium supplementation results in increased neural progenitor cell survival and neuronal-lineage differentiation in the hippocampus of young adult and aged mice. Ferroptotic cell death has been linked to the cell death that occurs in a number of neurodegenerative diseases and stroke. A key aspect of our future research program will be to investigate whether blocking ferroptotic cell death via dietary or environmental interventions can rescue the behavioural and cognitive decline observed in an animal model of stroke.