Macquarie University Research Finds Causes Of Protein Build-Up Could Help Develop Dementia Treatment

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

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.”

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