Judith Allen-Graham

Alfred Hospital - Monash University
Rotary Club of Crows Nest
Patricia Hooton Scholarship 2009
Alzheimer's Disease

Judith grew up in Lakes Entrance, Victoria.  She was awarded a Scholarship for Excellence and Equity from Monash University and moved to Melbourne to study a Bachelor of Biomedical Science. She received a Commonwealth Accommodation Scholarship from Monash University and completed her honours degree in 2007, investigating whether there is a link between Coelic’s Disease and Ataxia.
 
Judith’s Australian Rotary Health, Rotary Club of Crows Nest and Monash University Funding Partners PhD Scholarship project involves studying the role of Amyloid Precursor Protein (APP) and Amyloid Precursor-like Protein 2 (APLP2) in regard to Alzheimer’s disease. The exact role of APP is yet to be fully explained. It is known to be a key player in the pathogenesis of Alzheimer’s disease.
 
In 2008, Judith received a travel grant from Monash University to present her research project at the Society for Neuroscience Annual Conference in Washington DC. She also participated in a pre-conference satellite workshop for PhD students studying Alzheimer’s disease; an experience she reported as being particularly valuable.

SUMMARY OF PROJECT:
Inhibition of APP and APLP2 using siRNA to investigate protein function and Alzheimer’s disease
 
Alzheimer’s disease is the leading cause of dementia worldwide. As its occurrence increases rapidly with age, and life expectancy grows, Alzheimer’s disease has become a major public health problem.
 
One pathway identified in the development of Alzheimer’s disease is the splitting of a protein named amyloid precursor protein (APP) and the subsequent release of a toxic fragment known as b-amyloid (Ab). Ab is the main element of plaques found in the brains of people with Alzheimer’s disease.
 
This PhD project involves studying the role of APP and Amyloid Precursor-like Protein2 (APLP2) in Alzheimer’s disease.APLP2, a member of the same family of proteins, does not give rise to Ab neurotoxic fragments.
 
As Alzheimer’s disease is huge public health issue, therapies aimed at addressing the causes of the disease are important because they focus on prevention rather than symptomatic relief.  If it is proven that APLP2 can carry out an equivalent function to APP, then gene therapy aimed at decreasing APP in mature neurons can be pursued.