Dr Tara Walker

Research Fellow

Centre for Restorative Neuroscience
Queensland Brain Institute
t.walker1@uq.edu.au
+61 7 334 66498

Overview

Dr Tara Walker is a Senior Research Associate at the Queensland Brain Institute. Dr Walker's group is investigating the mechanisms governing the lifelong production of neurons in the adult brain (adult neurogenesis). Tara studied Biotechnology as an undergraduate at the Queensland University of Technology (Brisbane, Australia), before carrying out her PhD in the field of Plant Biotechnology. In 2003 she made the transition to neuroscience, joining the Queensland Brain Institute (QBI) and the group of Professor Perry Bartlett. Here she became interested in the field of adult hippocampal neurogenesis, particularly in its activity-dependent regulation. In 2010, she joined the group of Professor Gerd Kempermann at the Center for Regenerative Therapies in Dresden, Germany, where she was awarded a Marie Curie International Incoming Fellowship in 2011. In July 2018 she returned to QBI to take up a position in the newly developed Centre for Restorative Neurosciences as a Senior Research Associate, where she will apply her knowledge of neural stem cell biology to stroke research.

Research Impacts

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.

Qualifications

  • Doctor of Philosophy, Queensland University of Technology
  • Bachelor of Applied Science, Queensland University of Technology

Publications

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Available Projects

  • Atrophy following stroke results in various forms of cognitive decline. It has recently been demonstrated that following stroke a subset of cells die via ferroptosis, a newly-identified form of cell death. We hypothesise that blocking ferroptotic cell death will improve recovery in learning and memory and protect against cell loss following stroke. Our specific aims are to determine whether blocking ferroptotic cell death reduces the neuronal cell loss and cognitive decline: 1) following hippocampal stroke 2) following cortical stroke 3) in an aged model of stroke 4) in conjunction with a neuronal precursor survival cue such as environmental enrichment

  • The lifelong production of new neurons occurs in one important brain region, the hippocampus. This process however, significantly decreases with age and in several neurodegenerative diseases and results in a concomitant decline in associated learning and memory functions. We have recently shown that selenium can protect against ferroptosis, a recently identified form of cell death. We will investigate whether targeting this cell death pathway can prevent hippocampal neuronal loss and improve the associated cognitive function in the aged brain.

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Publications

Journal Article

Conference Publication

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • Atrophy following stroke results in various forms of cognitive decline. It has recently been demonstrated that following stroke a subset of cells die via ferroptosis, a newly-identified form of cell death. We hypothesise that blocking ferroptotic cell death will improve recovery in learning and memory and protect against cell loss following stroke. Our specific aims are to determine whether blocking ferroptotic cell death reduces the neuronal cell loss and cognitive decline: 1) following hippocampal stroke 2) following cortical stroke 3) in an aged model of stroke 4) in conjunction with a neuronal precursor survival cue such as environmental enrichment

  • The lifelong production of new neurons occurs in one important brain region, the hippocampus. This process however, significantly decreases with age and in several neurodegenerative diseases and results in a concomitant decline in associated learning and memory functions. We have recently shown that selenium can protect against ferroptosis, a recently identified form of cell death. We will investigate whether targeting this cell death pathway can prevent hippocampal neuronal loss and improve the associated cognitive function in the aged brain.