University of Tasmania, Australia

Senior Lecturer
Honorary Member and Fellow of the Menzies Research Institute of Tasmania

PhD

General Responsibilities

Dr Foa graduated from Deakin University with her PhD in 1996 and then spent 5 years in the US, working at the University of Michigan and Cold Spring Harbor Laboratory in New York. While there, she learnt a variety of in vivo and in vitro live cell imaging techniques that she now employs in her own laboratory at UTAS.

Dr Foa is responsible for the pre-clinical pharmacology teaching across the medical curriculum, and the teaching of developmental neurobiology in the Bachelor of Medical Research and related courses. She also teaches 3rd year research, honours and PhD students in her research laboratory, which she runs jointly with Professor David Small in the Menzies Research Institute.

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Teaching Responsibilities

I teach Pharmacology and Neuroscience. My principle teaching responsibility is pharmacology across years 1-3 of the medical course.

I coordinate CAM202 (second semester of second year medicine).

I also teach into the 3rd year Biomedical Neuroscience course, where I introduce students to current research in developmental neurobiology and learning and memory.

I regularly run third year research project students in my lab and also have Honours and PhD students who all work in Neuroscience research.

Units Taught

• CAM101 - Foundations of Medicine 1
• CAM102 - Foundations of Medicine 2
• CAM201 - Fundamentals of Clinical Science 1
• CAM202 - Fundamentals of Clinical Science 2
• CAM304 - Fundamentals of Clinical Science 3
• CAM305 - Functional Clinical Practice
• CHP311 - Neuroscience A
• CHP312 - Neuroscience B

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Publications

• Liu, S. J., Gasperini, R., Foa, L., & Small, D. H. (2010). Amyloid-beta Decreases Cell-Surface AMPA Receptors by Increasing Intracellular Calcium and Phosphorylation of GluR2. Journal of Alzheimer's Disease, 21(2), 655-666.
• Vincent, A. J., Gasperini, R., Foa, L., & Small, D.H. (2010). Astrocytes in Alzheimer’s disease: Emerging roles in calcium dysregulation and synaptic plasticity. Journal of Alzheimer's Disease, 22(3), 699-714.
• Klaver, D., Hung. A. C., Gasperini, R., Foa. L., Aguilar. M. I., & Small, D. H. (2010). Effect of heparin on APP metabolism and Abeta production in cortical neurons. Neurodegenerative Diseases, 7(1-3), 187-189.
• Foa, L. & Gasperini, R. (2009). Developmental roles for Homer: more than just a pretty scaffold. Journal of Neurochemistry, 108(1), 1-10.
• Small, D. H., Gasperini, R., Vincent, A. J., Hung, A. C., & Foa, L. (2009). The role of Aβ-induced calcium dysregulation in the pathogenesis of Alzheimer’s disease', Journal of Alzheimer's Disease, 16, 225-233.
• Gasperini, R. J., Choi-Lundberg, D., Thompson, M. J. W., Mitchell, C. B., & Foa, L. (2009). Homer regulates calcium signalling in growth cone turning. Neural Development, 4(29)

Web Access Research Portal (WARP)

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Additional Information

Research Interests

Our research looks at the basic question of how does the brain develop. The brain is an intricate precise electrical circuit, yet the exact mechanisms that control how brain circuits are connected remain a mystery. Our research centers on the role of calcium in growing nerve cells, or neurons.

We know that changes in levels of calcium within the cell are crucial to normal neuron function, and this is particularly true in young developing neurons. Our work focuses on how calcium is controlled in developing neurons, such that it can aid in neuronal growth and brain connectivity.

While the aim of our work is to contribute to the understanding of how the normal brain develops and functions, this information also contributes to an understanding of the cellular basis of disorders associated with brain development such as mental retardation, autism and schizophrenia.

The broader implications of our work relate to injury and neurodegenerative disease:

After injury, damaged neurons need to reconnect with their partner cells if functional recovery is to be restored. At present, neurons in our brain and spinal cord can’t regenerate at all, while neurons in our arms and legs can, but very very slowly. If we can understand how neurons grow during development, then perhaps we can exploit those mechanisms to improve neuron regeneration after injury and hence improve recovery.

Understanding the developing brain also has implications for the ageing brain. Current work suggests that some of the processes that are important for normal neuron growth during development may be activated inappropriately during neurodegeneration, leading to diseases such as Alzheimer's disease. Hence projects in our lab cover three main areas:

1. Fundamental development projects, where by we work to understand how the amazing human brain circuitry is wired up during development. Examples of these projects include:
   
   • The role of STIM1 in regulating calcium within the developing neuron
   • The role of Homer in axon pathfinding
2. Injury related projects whereby we study novel molecules or compounds that may be able to positively influence neuron growth and hence be useful in nerve regeneration after injury or disease;
3. Ageing related projects in which we investigate how ageing related insults damage neurons, disrupting communication between neurons, thought to be the cellular basis of our memories. An example of one of these projects is:
   
   • The role of Homer in calcium regulation in Alzheimers disease

In our Research, we use a combination of live cell imaging, calcium imaging, molecular biology and tissue culture approaches to decipher the basis of neuron-to-neuron connections.