Digitally created image of brain in skull

ForeFront

RESEARCH CENTRE

Our 5-year-plan

In five years we aim to have a number of novel models and target molecules for high-throughput intervention studies, and developed better diagnostic tools for identifying and tracking the underlying proteinopathy.

Our 5 year planYear 1 Aims
Clinics

Neuroimaging (Hodges) – establish the neural basis of on disinhibition, neuroendocrine changes and memory changes using cognitive and imaging approaches.
Electrophysiological tracking (Kiernan) – looking at the incidence, pattern, severity and functional significance of motor system involvement in FTD.
Neuropathology

Retrospective clinical analyses (Halliday and Hodges) – Postmortem cases will be stratified according to clinical syndromes.
Retrospective pathological analyses (Kril) – identify features predictive of the underlying pathology.
Biology

Molecular mechanisms of toxicity (Ittner) – determine the contribution to cell death induced by different species and mutant forms of tau, TDP43 and FUS.
Identifying genes that confer protection (Götz) – identify protective genes, and to determine which genes discriminate vulnerable from protected neurons.

 

Year 2 Aims
Clinics

Neuroimaging/connectomics (Hodges) – Progression in vivo of specific patterns of degeneration at different disease stages.
Electrophysiological tracking (Kiernan) – bvFTD will be longitudinally assessed using TMS.
Pathology

Quantifying degeneration in patients (Kril) – Tissue atrophy, type and severity of neuronal loss and inclusions.
Changes in protein levels as a read-out of disease progression (Halliday) – across different brain regions to determine the pattern of disease progression, and rate of change over the course of disease.
Candidate diagnostic approach (Halliday) – assess serum levels of the main pathogenic proteins involved in FTD/MND.
Biology

Changes in protein levels as a read-out of disease progression (Ittner) – vin multiple brain regions using tissue from validated animal models of progression.
Cell culture models of disease spreading (Ittner) – will identify the distinct tau protein species and mechanisms that promote spreading of pathology.
Forward genetics to identify disease modifiers (Götz) – use genome-wide ENU mutagenesis and mapping to reveal molecules that regulate neurodegeneration.

 

Year 3 Aims
Clinics

Neuroimaging (Hodges) – assess neural basis of more deficits using cognitive and imaging approaches.
Electrophysiological tracking (Kiernan) – The incidence, pattern, severity and functional significance of motor system involvement continued.
Clinical trial (Hodges and Kiernan) – develop the biomarker tool and collect baseline data for monitoring any change over the course of disease.
Neuropathology

Retrospective clinical analyses (Halliday and Hodges) – Postmortem cases will be stratified by pathology.
Retrospective pathological analyses (Kril) – identify features predictive of the underlying pathology.
Quantifying degeneration (Kril) – validate the rate of change in different brain regions to compare with animal models of progression.
Changes in tau protein levels (Halliday) – using fresh tissue from autopsy-confirmed patients to validate animal models of progression.
Validation in human tissues (Kril and Halliday) – assess genes that confer protection in animal models.
Biology

In vivo mouse models (Ittner) – develop novel in vivo models of pathological spreading along neuronal networks.
Cell culture models of disease spreading (Ittner) – identify the distinct TDP43 protein species and mechanisms that promote spreading of pathology.
The worm C. elegans as model system (Götz) – assess the integrity of neurons expressing abnormal protein inclusions.
Novel transgenic mouse models (Götz) – The mice will be analysed for phenotypic alterations, biochemically, behaviourallyand histologically.

Year 4/5 Aims
Clinics

Neuroimaging/connectomics (Hodges).
Motor as biomarker (Kiernan and Halliday).
Electrophysiological tracking (Kiernan).
Symptom management (Hodges and Kiernan).
Neuropathology

Quantifying degeneration (Kil).
Changes in tau protein levels (Halliday).
Candidate progression approach (Halliday).
Biology

Neuroprotection in C. elegans (Götz).
Validation of neuroprotective genes in mice (Götz).
Novel transgenic mouse models (Götz).
Clearing protein aggregates (Ittner).
In vivo mouse models (Ittner).
Interactome of candidate proteins (Ittner).
Combinatorial transgenics (Ittner).

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‘It is like they were miraculously healed!’’ Schizophrenia is diagnosed by clinical observation of behaviour and speech. This is why NeuRA researchers are working hard to understand the biological basis of the illness. Through hours of work and in collaboration with doctors and scientists here and around the world, NeuRA has made an amazing breakthrough. For the first time, researchers have discovered the presence of antibodies in the brains of people who lived with schizophrenia. Having found these antibodies, it has led NeuRA researchers to ask two questions. What are they doing there? What should we do about the antibodies– help or remove them? This is a key breakthrough. Imagine if we are treating schizophrenia all wrong! It is early days, but can you imagine the treatment implications if we’ve identified a new biological basis for the disease? It could completely change the way schizophrenia is managed, creating new treatments that will protect the brain. More than this, could we be on the verge of discovering a ‘curable’ form of schizophrenia? How you can help We are so grateful for your loyal support of schizophrenia research in Australia, and today I ask if you will consider a gift today. Or, to provide greater confidence, consider becoming a Discovery Partner by making a monthly commitment. We believe there is great potential to explore these findings. Will you help move today’s breakthrough into tomorrow’s cure? To read more about this breakthrough, click ‘read the full story’ below. You are also invited to read ‘Beth’s story’, whose sweet son Marcus lived with schizophrenia, by clicking here.
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