Neurodegenerative diseases are common and devastating age-related diseases with no effective disease-modifying treatments. For example, ~ 44 million people worldwide are afflicted by dementia and its prevalence is expected to triple over the next 40 years as people live longer. The need for a safe and efficient way to remove misfolded neurotoxic proteins implicated in many diseases of the central nervous system is urgent.
Alzheimer’s disease is the most common form of dementia. It is a degenerative brain condition, characterised by memory loss and increasingly impaired cognitive function. It is most commonly diagnosed in people over 65 years of age, although an early-onset variant may occur earlier.
The cost of Alzheimer’s disease in Australia is estimated at more than $3.6 billion per year. As our society ages, the burden of the disease on our society is increasing.
The cause of Alzheimer’s disease is not known, but there are a number of potential factors under investigation. The disease is characterised by the presence of plaques in the brain, made up principally of a peptide called Abeta which is a breakdown product of a protein called amyloid precursor protein (APP).
The long-term aim of Alzheimer’s disease research at SVI is to determine the structure of APP in order to understand its normal physiological function as a basis for structure-based drug design of anti-Alzheimer's drugs. In another approach we have investigated ways of clearing the toxic Abeta from the diseased brains using approaches including antibodies and host immune cells called microglia.
Along with colleagues at the Florey Neuroscience Institutes and Monash University, researchers in SVI’s Structural Biology Unit have identified a number of drugs which, based on their potential to bind to and inhibit a specific cellular receptor called IRAP, have potential to be enhancers of memory, and thus may represent a novel treatment for dementia.