A clever new therapy for preventing brain ageing and cognitive impairment in Alzheimer's Disease. Leveraging the discovery of a new mechanism of action, UNSW researchers established a proof of concept in animal model and demonstrated full protection from memory deficits.
This invention can shift the paradigm for treating patients with Alzheimer's disease, from managing symptoms to effectively halting the disease.
Alzheimer's disease damages the brain, resulting in impaired memory and behaviour. It is estimated that worldwide, nearly 44 million people have Alzheimer's or a related dimentia. (Alzheimer's Disease International). UNSW researchers are very excited about the new research that has closed the knowledge gap: "we have identified a novel molecular pathway that will allow therapies to stop disease progression" says Professor Lars Ittner
- New target (early in the signalling cascade)
- Novel Mechanism of Action (MoA)
- Proof of Concept in animal models
- Prevention of the disease and reduction of symptons
- New target and therapy for Alzheimer's disease
- New biomarker for Alzheimer's Disease
UNSW is seeking a partner to license this technology or to work with the researchers to further develop this technology. A provisional patent application was filed (No. 2016900764) in March 2016.
Researcher and Technical Details
Alzheimer’s disease brains are characterized by the deposition of two proteins; amyloid-beta in extracellular plaques and tau in intracellular tangles. The current understanding is that amyloid-beta is toxic to cells much before its deposition, causing neuronal dysfunction and death.Tau was thought to mediate the toxic effects of amyloid-beta on neurons, but it was only in 2010, when our researchers linked amyloid-beta and tau mechanistically, in what became a paradigm shifting publication in the top-ranked journal Cell.
However, it remained unclear how the process of amyloid-beta toxicity via tau is regulated and, more importantly, if such a regulation could be targeted therapeutically to prevent amyloid-beta toxicity and therefore cognitive deficits. Our new research has closed this gap; we have identified a novel molecular pathway that limits the neurotoxicity of amyloid-beta in Alzheimer’s disease.