Molecular Neurobiology: Small & Foa Group
Research in our laboratory is focused on identifying the molecular mechanisms that control brain development and ageing. In particular, our research aims to understand the signalling pathways that regulate neural stem cell behaviour, axon path-finding and synapse formation. Dysregulation of these processes has been demonstrated to contribute to nerve cell damage, leading to cognitive and motor deficits in patients suffering from diseases such as Alzheimer's disease and schizophrenia.
Development and ageing of the central nervous system is a complex, highly co-ordinated process. Cells within the brain re-wire their connections, and new cells are added to the brain throughout life. Each change is shaped by the interplay between genetic and environmental factors. Surprisingly, while the mature human brain contains trillions of neural connections, a relatively small number of genes control the way in which these connections are formed and modified. Defects or changes in protein expression cause dysfunction, which can lead to neurodegenerative disease later in life. Our research focus is to identify the fundamental mechanisms that cause brain diseases with the aim of identifying new drug targets. Our research also aims to discover biomarkers that can be used for the diagnosis of brain diseases.
A number of research projects are available for students who wish to pursue an Honours or PhD degree within our laboratory. Please contact Professor David Small (Neurodegeneration), Dr Lisa Foa (Neural Development) or Dr Kaylene Young (Glial Research) for more information.
- Mechanisms that Control the Progression of Alzheimer's Disease
- The role of store-operated calcium entry in neuronal development
- Examining the role of the amyloid precursor protein of Alzheimer's disease in normal CNS function
Related Funding Bodies
- Lila Landowski (PhD Student)
- Dr Rob Gasperini (Research Fellow)
- Dr Katherine Southam (Research Fellow)
- Dr Marta Bolos (Research Fellow)
- Dr Adele Vincent (Research Fellow)
- Yanling Hu (PhD Candidate)
- Professor Mibel Aguilar - Monash University
- Dr Craig Freeman - Australian National University
- Dr Lisa Martin - Monash University
- Professor Chris Parish - Australian National University
- Associate Professor Helena Parkington - Monash University
- Professor Dudley Strickland - University of Maryland, USA
- Dr Javier Saez-Valero
- Professor Paul Worley - Johns Hopkins, USA
- Mitchell CB*, Gasperini RJ*, Small DH*, Foa L* (2012). STIM1 is necessary for store-operated calcium entry in turning growth cones. J Neurochem. doi: 10.1111/j.1471-4159.2012.07840.x.
- Cui H*, Hung AC, Freeman C, Narkowicz C, Jacobson GA, Small DH* (2012). Size and sulfation are critical for the effect of heparin on APP processing and AB production. J Neurochem. doi: 10.1111/j.1471-4159.2012.07929.x.
- *Vincent AJ, *Gasperini R, *Foa L, *Small DH. Astrocytes in Alzheimer's disease: emerging roles in calcium dysregulation and synaptic plasticity. Journal of Alzheimer's Disease 2010; 22:699-714.
- *Gasperini R, *Choi-Lundberg D, Thompson MJW, Mitchell CB, *Foa L. Homer regulates calcium signalling in growth cone turning. Neural Dev. 2009. 4:1.08
- Petratos S, Li QX, George AJ, Hou X, Kerr ML, Unabia SE, Hatzinisirioui I, Maksel D, *Small DH. The β-amyloid protein (A&beta) of Alzheimer's disease increases CRMP-2 levels and phosphorylation through a Rho-GTPase-dependent mechanism thereby inhibiting tubulin assembly in neurons. Brain 2008; 131, 90-108.
- *Small D H. Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression? Trends in Molecular Medicine 2008; 14, 103-108.
* Denotes Menzies Researcher