ABOUT THE GRANT AND AWARD WINNERS

Since its establishment in 1978, the Sir Zelman Cowen Universities Fund has raised funds for medical and scientific research focused on finding therapies for still-incurable diseases. The work supported by the Fund is carried out at the University of Sydney and the Hebrew University of Jerusalem.

Since the launch of its Alzheimer's Disease & Inflammation Initiative in 1996, the Fund has supported research aimed at finding the cause and a potential cure, for the dementia of Alzheimer's disease (AD).

Following this interest, in May 2008, the Trustees of the Fund announced the establishment of the Sir Zelman Cowen Universities Fund Alzheimer's Disease Research Grant for a research project in the field of Alzheimer's disease, where the aim of the project is to develop and/or assess new treatments for this condition. A call for applications was also made at this time to permanent members of staff of the University of Sydney and the Hebrew University of Jerusalem. Joint applications for cooperative projects between permanent members of staff of both universities were also welcomed.

In September 2008 the Trustees of the Fund announced the award of the grant of $100,000 over 2 years to Dr Claire Goldsbury, Brain & Mind Research Institute, University of Sydney and Dr Karen Cullen, Discipline of Anatomy & Histology, University of Sydney for their project entitled, Energy deficiency as a cause of neuritic pathology in Alzheimer's Disease.

Summary of the Project:
Alzheimer's disease (AD) progressively destroys brain cells involved in memory functions. One of the diagnostic abnormalities of the damaged nerve cells is their accumulation of a protein called tau. Tau inclusions may contribute to nerve cell dysfunction by blocking trafficking of important components to synapses. Loss of synapses underlies the memory loss central to the disease. This project focuses on the process that causes the accumulation of tau. Understanding this process is important for identifying and developing new ways to treat AD.

Decline in energy metabolism, visible in AD brain scans occurs in the same areas as damaged nerve cells. The hypothesis on which this project is based is that reduced energy metabolism in the brain initiates the accumulation of tau. Using a multi-pronged approach, this study aims to determine ways to short-circuit the pathway between energy depletion and brain damage by revealing the sequence of events that explains the abnormal accumulation of tau.

For further information about the AD Grant and this project, please contact the Fund's office.