Causes of protein build-up could help develop dementia treatment

Date
3 August 2023
Faculty
Faculty of Medicine, Health and Human Sciences

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For the first time, a team of researchers has uncovered possible causes for the build-up of tau protein in the brains of patients with a rare neurodegenerative disease – and the discovery could have important implications for Alzheimer’s and other forms of dementia.

Researchers from Macquarie University, with colleagues from the University of Toronto and Mohammed Bin Rashid University of Medicine and Health Sciences in Dubai, achieved the breakthrough while focused on the late-onset neurological disorder, progressive supranuclear palsy (PSP).

Similar to Parkinson’s disease, PSP is caused by the death of cells in brain regions important for coordinating movement and behaviour. This can result in problems with walking, balance, speech and eye movements.

There is currently no treatment for PSP, and most patients have just six to eight years to live from the time of diagnosis.

Microtubule-associated protein tau (MAPT) is associated with PSP and dementia when it accumulates abnormally in and clogs neurons and the glial cells that surround and support them.

Tau proteins are essential to the healthy functioning of the brain, but when too much is being produced, it can become pathogenic.

MAPT is a major focus for the Macquarie University Dementia Research Centre (DRC), including the development of potential therapies aiming to either eliminate the build-up of MAPT or reduce its production in the brain.

DRC Research Fellow and lead author Dr Shelley Forrest says the findings of this latest study, published in Acta Neuropathologica, are very exciting.

“We focused on the RNA that is translated to the tau protein, and we’ve been the first to demonstrate that tau RNA is expressed in the supporting glial cells as well as in the neurons,” she says.

“Nobody has been able to previously identify why abnormal tau protein accumulates, but we have been able to highlight two potential pathways for the transmission and accumulation of tau in these brain cells, and its spread through the brain.

“This raises the possibility of developing two-pronged therapy strategies for pathogenic tau that would attack both pathways at once instead of only one or the other.

“It opens up a novel insight into the disease cause of PSP, and potentially other tau-related diseases such as Alzheimer’s as well.”

The three-year study was funded by an Australian National Health and Medical Research Council Ideas Grant.

Read the paper.

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Media Contact

Georgia Gowing

georgia.gowing@mq.edu.au

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