Alzheimer therapy not far-off

Australian researchers have discovered how a protein called TAU affects and mediates the toxicity of amyloid-b, which together with TAU, cause the symptoms of Alzheimer’s disease.

The groundbreaking new study led by Professor Jürgen Götz and Dr Lars Ittner, based at the University of Sydney’s Brain and Mind Research Institute (BMRI), has been published in the international scientific journal, Cell.

Professor Götz said this significant breakthrough made by Dr Ittner and their team, has implications for how the disease develops and how it may be treated.

“Alzheimer’s disease is a major health threat to Australia’s ageing population,” he said.
 
“A handful of approved drugs provide if at all only very modest symptomatic relief, without curing the disease. Therefore, to develop effective treatments, it is absolutely necessary that the basic mechanisms underlying these disorders be understood. This was our challenge.”

The brain of all Alzheimer’s patients is characterised by two types of insoluble deposits; amyloid-b plaques and neurofibrillary tangles, the latter formed by the protein TAU.

The research findings challenge the accepted research paradigm.

The researchers found that TAU is essential for the positioning of yet another protein, the kinase FYN, at the dendritic site of the synapse, which then renders the neuron vulnerable to amyloid-b.

“By genetically deleting TAU or introducing a non-functional variant of TAU, we found we could prevent the development of symptoms in mouse models of Alzheimer’s disease.”

“These mice showed normal survival and their memory appeared to be perfectly fine.”

In the second part of the study, Professor Götz and Dr Ittner explored the potential of their discovery for a treatment of Alzheimer’s disease.

“We translated our findings into a novel therapeutic approach by using a small peptide that mimics the effects of removing TAU from the synapse, and we were thrilled to see that this not only fully prevented the pathology in our Alzheimer’s disease models but cleared their memory deficits,” Dr Ittner said.

“Although there is still a long way to go we believe we may have found a way of treating Alzheimer’s disease,” adds Professor Götz.

This breakthrough has encouraged Professor Götz and Dr Ittner in their endeavours to find a cure for Alzheimer’s disease.