Visitors to QBI on 2013 Dementia Awareness Day  discuss the topic with researcher Tishila Palliyaguru.

Without the support of QBI’s friends and donors, the significant discoveries we have made during the past 12 months, some of which are highlighted below, would not have been possible. 

We are confident that we will continue to make new discoveries, but your contributions will more rapidly assist with completion and clinical translation.

To donate please visit www.qbi.uq.edu.au/how-to-donate-to-qbi

MRI scans being used as a diagnostic tool for Alzheimer’s detection 

Scientists may now be able to detect early features of Alzheimer’s disease using magnetic resonance imaging (MRI).

Using MRI, Associate Professor Elizabeth Coulson and her team were able to detect degeneration of basal forebrain cholinergic neurons – an early and key feature of Alzheimer’s disease. 

“Traditional methods of detecting changes to the brain in Alzheimer’s disease by MRI require tissue to have undergone significant degeneration such that there is atrophy or loss of the tissue, ” says Associate Professor Coulson.

Her team has now determined that early neurodegenerative changes in the basal forebrain can be detected in an animal model using a non-invasive method of MRI called diffusion tensor imaging (DTI).

“By doing this, we were able to pinpoint significant signs of Alzheimer’s onset, before the basal forebrain cells had actually deteriorated,” Associate Professor Coulson said.

“This could allow patients the opportunity to receive treatment to either reduce the effects or cease the onset of Alzheimer’s.” 

Scientists are now looking to use DTI to detect these early signs of Alzheimer’s disease in humans. 

“These findings provide increased support for using DTI and probabilistic tractography for diagnosing and/or monitoring the progression of conditions affecting the integrity of the basal forebrain cholinergic system in humans, including Alzheimer’s disease,” Associate Professor Coulson said. 

Scientists clearer on gene linked to motor neuron disease

QBI’s scientists are closer to developing a therapeutic target for neurodegenerative disorders, including motor neuron disease (MND).

The study monitored the functions of the protein TDP-43 in the nervous system, which until now have been largely unknown.

An expert in MND and contributor to the study, Dr Marie Manglesdorf, says the analysis produced a list of 1,839 potential TDP-43 gene targets, many of which overlap with previous studies.

“In the past we have known TDP-43 is an RNA binding protein involved in gene regulation through control of RNA transcription, splicing and transport, however, we haven’t been able to precisely pinpoint the genes it controls,” Dr Mangelsdorf said.

“By understanding the role TDP-43 plays in maintaining connections between nerve and muscle cells and the genes it controls, we can work towards developing therapeutic interventions to delay or eliminate deterioration of the gene.”

QBI’s research into MND is made possible thanks to the Ross Maclean Senior Research Fellowship, the Peter Goodenough Bequest and the MND and Me Foundation Ltd.

New insights into learning and memory

Work from Professor Perry Bartlett’s laboratory has shown, for the first time, that the brain cells usually responsible for mediating immunity, microglia, have an inhibitory effect on memory during ageing.

The discovery, published in The Journal of Neuroscience, came after postdoctoral researcher Dr Jana Vukovic observed that the increased production of new neurons in mice that were actively running was due to the release of fractalkine in the hippocampus – the brain structure responsible for specific types of learning and memory.

Professor Bartlett said it had been known for some time that exercise increased the production of new nerve cells in the hippocampus in young and even aged mice.

“But this study found that it is fractalkine that appears to be specifically mediating this effect by making the microglia produce factors that activate the stem cells that produce new nerve cells,” he said.

“Once the cells are activated they divide and produce new cells, which underpin the animal’s ability to learn and form memories. This means that fractalkine may form the basis for the development of future therapies.

“The discovery is especially exciting because we have found that older animals suffering cognitive decline showed significantly lower levels of fractalkine.

“We are seeking ways of increasing fractalkine levels in patients with cognitive decline, and hoping this may be a new frontline therapy in treating dementia.”

Dr Vukovic said that until relatively recently, it was thought the adult brain was incapable of generating new neurons.

“But work from Professor Bartlett’s laboratory over the past 20 years has demonstrated that the brains of adult animals retain the ability to make new nerve cells,” she said.

“The challenge is to find out how to stimulate this production in the aged animal and human where production has slowed.”

The latest work was a significant step toward understanding the molecular mechanism that may impair learning and memory in the ageing population.