" In their study, the researchers discovered that a crucial step that leads to Alzheimer’s disease pathology, known as tau tangles, may be misunderstood and not as bad as first thought. "
The ‘new’ role of tau in Alzheimer’s progression

The role of a toxic protein, called tau, suggested responsible for the progression of Alzheimer’s disease, has been challenged by Sydney-based researchers at Neuroscience Research Australia (NeuRA), who have shed new light on its process.

In their study, published in the Journal Science, the researchers discovered that a crucial step that leads to Alzheimer’s disease pathology, known as tau tangles, may be misunderstood and not as bad as first thought.

It has been previously noted that amyloid-beta proteins cause a modification (known as phosphorylation) to the tau protein resulting in cell death and, ultimately, Alzheimer’s disease symptoms. Increased phosphorylation of tau eventually leads to its accumulation as tangles. However, results from this new study suggests that the phosphorylation of tau initially has a protective effect on neurons, and that amyloid-beta assaults this protective functionality until it is progressively lost.

“This study has completely changed our understanding of what happens in the brain during the development of Alzheimer’s disease,” said study leader, Professor Lars Ittner.professor-lars-ittner-neura

Professor Ittner and his research team specifically identified a protein kinase, called p38y, which mediated (or lessened) tau phosphorylation. They noted that when it was depleted it exacerbated neuronal activities and cognitive deficits in the mice, whereas when it was increased, these deficits were not seen.

Professor Ittner also stated they used human brain tissue (donated through the Sydney Brain Bank) to identify the protein in question, which led them to the further studies in mice to confirm their discovery.

“This is a completely new mindset, that the reason tau becomes modified is actually to protect from damage.

“We found that p38γ, which initially offers protection, fades away early in the brains of people with Alzheimer’s disease, suggesting a loss of protection.

“Part of our study involved reintroducing p38γ and increasing its activity. We saw that, in mice, it could prevent memory deficits from happening, so it has true therapeutic potential. If we can stimulate that activity, we may be able to delay or even halt the progression of Alzheimer’s disease,” said Professor Ittner.

What next?

This is one of the first studies to challenge the role of tau in Alzheimer’s disease and suggest it may not be completely responsible for neuronal damage, and in fact, quite the opposite. While this new discovery needs validation, it could potentially lead towards the development of new treatments and therapies for humans with Alzheimer’s disease. The researchers plan on progressing their findings through further studies and we’ll keep you posted.

 Posted: November 30th, 2016
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