What is dementia?
Dementia is not a single disease but rather a term to describe a number of illnesses that predominantly affect people over the age of 65. It is important to remember that not all older people get dementia. It is not a normal part of ageing. Dementia is a progressive brain disorder that affects a person’s ability to function normally. The condition involves the degeneration of brain cells, with common symptoms including memory loss, confusion, personality change, withdrawal and a loss of ability to do everyday tasks.
There are many different forms of dementia. The most common types of dementia are Alzheimer’s disease, vascular dementia, Parkinson’s disease, Dementia with Lewy bodies, Fronto Temporal Lobar Degeneration, Huntington’s disease, Alcohol related dementia (Korsakoff’s syndrome) and Creutzfeldt-Jacob disease.
Ageing dementia is one of the country’s most pressing health problems. Alzheimer’s affects more than two-thirds of dementia patients, and approximately a quarter of a million Australians. The total number of dementia cases in Australia is expected to rise to 900,000 by 2050. It presents significant challenges to the health care system, which makes directed research programs aimed at preventing and treating ageing dementia all the more urgent.
What can be done to help?
Currently there is no prevention or cure, however some medications reduce some of the symptoms. Enquiries on current clinical trials of new medications can be forwarded to Liz Arnold, Discipline of Psychiatry, School of Medicine, The University of Queensland, K Floor, Mental Health Centre, RBWH Herston Qld 4029, Tel: + 61 7 3365 5147, Email: firstname.lastname@example.org
National Dementia Helpline on 1800 100 500 QLD: email@example.com
The National Dementia Helpline is a telephone information and support service available across Australia. The Helpline is for people with dementia, their carers, families and friends, as well as people concerned about memory loss. It is also used by health professionals, service providers, community organisations and students.
Alzheimer’s Australia Queensland: https://qld.fightdementia.org.au/
Alzheimer’s Australia (Qld) offers a range of services for people with dementia, family carers, industry workers and anyone who wants to know more about memory loss, dementia or good brain health.
Promising new external drug developments: New Drug May Slow Alzheimer's Decline By 30%: www.bbc.com/news/health-33617141
Our Research - Ultrasound breakthrough to treat Alzheimer’s disease
Led by Professor Jürgen Götz, CJCADR scientists are developing a non-invasive ultrasound technology to treat Alzheimer’s disease and restore memory. The approach temporarily opens the blood brain barrier, activating mechanisms that clear toxic protein clumps and restoring memory functions. Research has been conducted in mouse models and is being scaled up in higher animal models. Human clinical trials are two-three years away.
Findings of the research, “Scanning ultrasound efficiently removes amyloid β and restores memory in an Alzheimer’s model”, are published in the journal Science Translational Medicine.
- News story link: Alzheimer’s breakthrough uses ultrasound technology.
- Interview about research: ABC Radio National.
CJCADR Group Leaders and Research
Professor Jürgen Götz is the inaugural Director of CJCADR. He has a major interest in dissecting pathomechanisms in neurodegenerative diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), and to exploit this molecular insight for the development of therapies. He and his team use genetically modified model organisms and are currently employing novel gene editing methods to improve these models. Key molecules of interest are tau, kinases such as Fyn and Pyk2, and amyloid-beta. Therapeutic strategies include small molecules, antibodies and peptides. The laboratory also tries to understand selective vulnerability in human neurodegenerative diseases, and is improving methods to deliver therapeutic agents past the blood-brain barrier.
Professor Perry Bartlett and his team played a significant role in overturning the dogma that the brain was unable to produce new neurons. His group is now dedicated to understanding the mechanisms that drive the continuous production of new neurons in a region of the adult brain known as the hippocampus. This process, called neurogenesis, slows as we age, and this loss of neurons has been associated with a loss of cognitive function. Professor Bartlett’s laboratory has identified several factors, including Wnt3a and prolactin, which upregulate neurogenesis in the hippocampus. These discoveries provide the prospect that therapeutics can be developed to reverse cognitive decline in the compromised, ageing brain.
Professor Elizabeth Coulson is revealing why certain neurons die in AD and how that affects cognition. Her work focuses on the p75 neurotrophin receptor and its role in neuronal loss. By blocking signalling through this receptor, nerve cell degeneration in the basal forebrain, which is induced by the neurotoxin amyloid beta, could be prevented. Using a novel spatial memory task, Professor Coulson and her team are currently testing whether basal forebrain degeneration, as measured by magnetic resonance imaging, correlates with or precedes spatial memory decline in humans (measures that could be used as biomarkers for dementia), and whether such changes can be reversed in animal models by blocking p75.
Dr Victor Anggono has a major interest in two neuronal receptors that are affected in the early stages of AD, the AMPA and the NMDA receptor. Both receptors play a crucial role in neuronal communication. Dr Anggono and his team address the central question of how signalling through the AMPA and NMDA receptors are regulated by disease processes. Dr Anggono further addresses the role posttranslational modification, in particular ubiquitination, has in neuronal functions.
Dr Zhitao Hu uses the round worm C. elegans as a genetic model to study the molecular mechanism of neurotransmission and neural circuit. Synaptic vesicle release is directly related to nervous system function. His long-term goal is to dissect the molecular mechanism of synaptic transmission. He is focusing on two aspects: release kinetics and release forms (spontaneous evoked release), using genetics, molecular biology, imaging and electrophysiology.
Associate Professor Massimo Hilliard uses the nematode C. elegans, a highly versatile model organism, to understand the role of the protein TDP-43 in motor neuron disease (MND). TDP-43 is a protein found in large clumps in patients with MND and some forms of frontotemporal dementia, and dysfunction in this protein is believed to cause abnormal processing of RNA. Associate Professor Hilliard uses C. elegans to test if and how the mutated form of TDP-43 disrupts RNA processing of molecules that are required at the synapses and neuromuscular junctions.
Professor Frederic A. Meunier’s laboratory is determined to discover how brain cells communicate and survive in health and disease. His laboratory focuses on the molecular events governing vesicular trafficking within presynaptic nerve terminals and neurosecretory cells. The discoveries that have come from the Meunier laboratory have led to a deep understanding of how secretory vesicles interact with the cortical actin network on their way to fuse with the plasma membrane to release the neurotransmitter. Professor Meunier and his team are interested in developing strategies to target trafficking events to reduce inflammation in the central nervous system with a focus on blocking the trafficking of the cytokine Tumour necrosis factor alpha (TNFalpha), one of the key molecules driving the development of a variety of neurodegenerative diseases including AD.
Keep up to date
To keep up to date with research developments at QBI:
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Queensland Brain Institute
The University of Queensland
St Lucia, QLD 4072
Phone: +61 7 3346 6300
Fax: +61 7 3346 6301