Kate Roberts

University of Wollongong, NSW
Rotary District 9680
Motor Neuron Disease 2011
Kate Roberts is a local of the Wollongong area and after attending the local public high school was accepted into the University of Wollongong to study a Bachelor of Science with a major in biology. She performed well at the undergraduate level exceeding entry requirements for acceptance into the school’s Honours program.
 
For Honours she secured a research project supervised by Dr Justin Yerbury involving research into an inherited form of motor neurone disease. Kate was able to contribute new knowledge to this important area and as a result found this honours year very rewarding.
“I was attracted to this area of research as my grandfather passed away from motor neurone disease before I was born. More than 20 years on there is still no cure for this disease. This deadly disease has such a significant impact on both suffers and their families. There is a great need for further scientific research to better understand this disease.” said Ms Roberts
 
With the Australian Rotary Health Scholarship she can now continue this important work with Dr Justin Yerbury as a PhD candidate at the Illawarra Health and Medical Research institute at the University of Wollongong. 
 
SUMMARY OF PROJECT:
Elucidating the role of extracellular mutant SOD1 in activation of glial cells and motor neurone cell death in ALS.
This project aims to determine how a genetic defect in the protein superoxide dismutase (SOD) affects immune processes implicated in Motor Neurone Disease. Novel approaches will be used to study how SOD activates immune cells both in the test tube and in animal models. The outcomes will provide new understanding of these processes and may contribute towards the ultimate development of new therapies.
  
Specific Aims
In order to more fully characterize the role of extracellular mSOD1 in ALS and to test the above hypothesis the current proposal will address the following aims:
 
1. Determine how mSOD1 activates microglia and astrocytes. An array of in vitro assays will be conducted to determine which receptor(s) and signal transduction pathways are responsible for mSOD1 activation of microglia and astrocytes. Including the first ever assays testing whether extracellular mSOD can activate astrocytes.
 
2. Determine if there is any relationship between SOD1 mutation, aggregation and ability to activate glial cells. Biophysical and cell culture methods will be employed to test whether there is a relationship between the mutation of SOD1, its propensity to aggregate, and its ability to activate glial cells.
 
3. Establish if extracellular mSOD1 mediates activation of microglia/astrocytes and toxicity in vivo. To examine the role of mSOD1 in triggering disease, recombinant mSOD1 protein will be infused into the spinal column of G93A transgenic mice (and control mice) prior to disease onset.