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Credit: Trends Update

Researchers at Sydney University's Brain and Mind Research Institute have discovered the way the protein named TAU influences and mediates the toxicity of amyloid-b, which together triggers the symptoms of Alzheimer's diseases.

The new study led by Professor Jurgen Gotz and Dr Larz Ittner has found significant understanding of the mechanism of the disease's progression and can affect the future's treatment of the disease.

Professor Gots said, Alzheimer's disease is a major health threat to Australia's aging population.

More than 250,000 Australians are currently diagnosed with dementia, with numbers reaching epidemic proportions. Of all diseases with a memory loss, Alzheimer's is the most prevalent, predicted to affect one in 85 people globally by 2050.

Alzheimer's is characterized by a progressive loss of cognition, followed by aggression and mood disturbance, and could eventually result in patients being institutionalized. Prof Gotz said the stress of the disease on patients, their families and caretakers is enormous.

Currently, the cure for the disease is still an elusive one.

Treatments that are available to date only provide modest symptomatic relief, without actually treating the disease and thus, the development of effective treatments depend absolutely on the right understanding of the mechanism underlying the disorder. With this in mind, the team of scientists dived into their study.

There are two types of insoluble deposits in the brain of all Alzheimer's patients - the amyloid-b plaques and the neurofibrillary tangles; which are formed by the protein TAU.

The link between the two types of deposits, said Prof Gots, was the key to understanding the disease. And successfully, the scientists found that TAU is essential for the positioning of 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.

The second part of the breakthrough study then involved exploring modes of treatment based on the new discovery of the role of TAU.

Dr Ittner said, 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.