An Honours degree is a year-long independent research project that can be done following the successful completion of a Bachelor's degree. Students spend the year in a laboratory in their chosen field conducting research and producing a thesis under the supervision of an academic staff member. An Honours degree allows students to deepen their understanding of a research topic through intensive practical work. Employers regard an Honours degree as a significant indicator of achievement and potential, and it may pave the way for entry into a Masters, MPhil or PhD program.
Students may undertake their Honours project supervised by researchers at QBI after gaining enrolment through one of the University's teaching schools. For students interested in applying for an Honours project in the neuroscience field, application can be made through the School of Biomedical Sciences (SBMS); more information about enrolment is available here.
Students approved to undertake an Honours project based at QBI must also apply directly to the Institute for building access, complete OHS training prior to commencing project work and agree to a Student Intellectual Property and Confidentiality Deed (contact QBI for more information by emailing collaborators@qbi.uq.edu.au).
Participation in an Honours project at QBI allows students to engage with and experience the rich intellectual resources and facilities of the Institute.
Current projects
Synaptic Functions
Group Leader Dr Victor Anggono v.anggono@uq.edu.au
Regulation of glutamate receptor membrane trafficking in neurons
The amino acid glutamate is the major excitatory neurotransmitter in the brain. The AMPA- and NMDA-type glutamate receptors are the principal receptors that mediate the majority of excitatory synaptic transmission in the mammalian brain. The dynamic trafficking and proper synaptic targeting of these receptors are crucial for synaptic plasticity, learning and memory. Importantly, dysregulation and aberrant trafficking of glutamate receptors have been implicated in many neurological disorders, including epilepsy, Alzheimer’s disease, schizophrenia and depression. In this project, we seek to determine the roles of glutamate receptor interacting proteins and post-translational modifications in regulating their precise membrane trafficking in mammalian central neurons.
Group Leader Dr Victor Anggono v.anggono@uq.edu.au
Epitranscriptomic regulation of neuronal plasticity
The human brain contains billion of neurons that are interconnected and highly organised into ensembles of neural circuits. The ability of neurons to modulate the number and strength of neuronal connectivity, termed synaptic plasticity, is critical during development, learning and memory. It is well established that activity-dependent gene transcription and de novo protein synthesis are required for long-term neuronal plasticity and memory consolidation. In this project, we seek to determine the role of post-transcriptional RNA methylation in shaping the transcriptomic and proteomic landscapes in neurons during synaptic plasticity.
Group Leader Professor Fred Meunier f.meunier@uq.edu.au
The overall goal of our research is to determine how brain cells communicate and survive in health and disease. Our lab focuses on the molecular events governing vesicular trafficking within presynaptic nerve terminals and neurosecretory cells. Our discoveries 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. In parallel to this process, internalisation of key neurotrophic factors occur at the synapse leading to survival. How these two trafficking pathways talk to each other is the focus of our current research. We have a range of projects available to honours looking at how molecular interactions govern trafficking events in synapse leading to both neurotransmission and survival.
Group Leader Dr Zhitao Hu z.hu1@uq.edu.au
Information processing in the nervous system is essential for brain function, and is predominantly determined by communication between neurons, which is achieved by the release of neurotransmitters from synaptic vesicles (SVs) at presynaptic nerve terminals. Since Katz and his colleagues first revealed that Ca2+ triggers neurotransmitter release by stimulating ultrafast SV fusion at the presynaptic terminal, studies have been focusing on the roles of synaptotagmin proteins in SV exocytosis. Synaptotagmins comprise a large family of membrane proteins with multifunctional C2 domains (C2A and C2B). Upon binding Ca2+, the C2 domains insert into the plasma membrane, and promote SNARE-mediated membrane fusion. Loss of function of synaptotagmins leads to severe brain dysfunction, with mutations being implicated in many neurological disorders such as epilepsy, Parkinson’s disease, and neuromuscular junction disorder. Despite the work done on synaptotagmins, a number of questions remain unresolved regarding their roles in synaptic transmission. How many synaptotagmins serve as Ca2+ sensors in neurons? How do synaptotagmins trigger fusion at the molecular level? What are the functional differences between distinct synaptotagmins and what causes these differences? How do synaptotagmins cooperate in SV fusion? What are the functions of synaptotagmins in other tissues? Addressing these questions is critical to elucidate the fundamental mechanisms of brain function, and the basis of synaptotagmin-related neurological disorders. We hope you can join our lab to work on these interesting and important questions.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Dr Pranesh Padmanabhan p.padmanabhan@uq.edu.au
Dissecting signalling crosstalk at the synapse
The brain is considered to be the last frontier, in terms of both understanding how it operates under normal and pathological conditions, and accessing it for therapeutic intervention. The NMDA receptor has a major role in learning and memory, functions which are impaired in AD. We have previously shown that Fyn is targeted to dendritic spines in a Tau-dependent manner, phosphorylating the NR2b subunit of the NMDA receptor, which allows the formation of an excitotoxic complex through which Abeta signals, causing downstream toxicity. Interestingly, STEP antagonizes Fyn, leading to internalization of NMDA receptor complexes. Additional targets of STEP include Fyn and Pyk2 that are inactivated by dephosphorylation of regulatory tyrosines within their activation loop, thereby modulating downstream signalling pathways. Because Abeta can activate both Fyn and STEP, this creates the paradoxical situation whereby Abeta could activate and at the same time inactivate Fyn, via activation of STEP. Fyn and STEP also have opposite effects on NMDA receptor activity, so the net effect of Abeta on NMDA receptor activity should be zero. However, one can speculate that the activation of Fyn and STEP does not occur at the same time. This Honours project is about gaining insight into Fyn, STEP and Pyk2 activation in response to Abeta using primary cultures, cell culture systems and a range of microscopy techniques.
Neurogenesis and Neuronal Survival
Group Leader Dr Tara Walker t.walker1@uq.edu.au
Can platelet factor 4 (PF4) reverse neurodegeneration and cognitive decline in Alzheimer’s disease?
Aging changes the adult brain at the molecular, cellular and functional levels, driving cognitive impairments and susceptibility to dementia-related neurodegenerative disorders, such as Alzheimer’s disease. Considering the rate at which the human population is aging, it is imperative to identify novel means to maintain functional integrity in the aged brain by protecting against, or even counteracting, the effects of aging. We have recently identified platelet factor 4 (PF4) as a key mediator of the rejuvenating effects of exercise on neurogenesis and age-related cognitive decline. This raises the exciting possibility that the rejuvenating effects of PF4 may extend beyond normal aging towards reversing neurogenic and cognitive decline in the context of Alzheimer’s disease. To investigate the therapeutic potential of PF4 administration on Alzheimer’s disease progression the well characterized transgenic AD mouse model APPSWE/PS1ΔE9 (APP/PS1) will be used. PF4 or saline will be systemically administered into the lateral tail vein of 12-month-old APP/PS1 or wild-type littermate mice every 3 days for 24 days. Proliferating cells will be labelled with a single BrdU injection given immediately prior to the first PF4 injection. Hippocampus-dependent learning and memory will be examined using the Novel objection location and APA paradigms. Following behavioral testing, regenerative capacity, neurodegenerative pathology and neuroinflammation in the hippocampus will be assessed using immunohistochemistry and confocal microscopy or western blot analysis.
This project is suited for student with a background in molecular biology and/or an interest in neuroscience.
Group Leader Professor Helen Cooper h.cooper@uq.edu.au
The adult brain contains neural stem cells that continue to make new neurons throughout life. Research in the Cooper lab has identified signaling molecules that may be harnessed to promote the birth of new neurons and their migration to damaged regions of the brain. The development of effective endogenous stem cell-based therapeutic strategies to promote neurogenesis and migration would be a major step forward in achieving functional recovery in the damaged brain.
Group Leader Professor Fred Meunier f.meunier@uq.edu.au
The overall goal of our research is to determine how brain cells communicate and survive in health and disease. Our lab focuses on the molecular events governing vesicular trafficking within presynaptic nerve terminals and neurosecretory cells. Our discoveries 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. In parallel to this process, internalisation of key neurotrophic factors occur at the synapse leading to survival. How these two trafficking pathways talk to each other is the focus of our current research. We have a range of projects available to honours looking at how molecular interactions govern trafficking events in synapse leading to both neurotransmission and survival.
Neuronal Development and Connectivity
Group Leader Professor Helen Cooper h.cooper@uq.edu.au
Investigating the mutations in genes that impact cortical development
The intricate neural architecture of the 6-layered mammalian neocortex is dependent on the ability of neural stem cells to differentiate into new neurons. These young neurons must then migrate into the correct cortical layers. In humans, mutations in genes controlling these processes have severe consequences for cortical development leading to intractable epilepsy, mental retardation, schizophrenia, dyslexia and autism.
Identifing molecular targets for axon regrowth
The corpus callosum is the major axon tract connecting the left and right hemispheres in the human neocortex. There are more than 50 different human congenital syndromes, often associated with mental retardation and epilepsy, in which this axon tract fails to develop. This project aims to identify molecular targets that can be manipulated to encourage axon regrowth and correct pathfinding in the damaged human brain and spinal chord.
Group Leader Professor Geoffrey Goodhill g.goodhill@uq.edu.au
Investigating the rules developing axons use to respond to both single and multiple molecular guidance cues
We are developing new microfluidic gradient technologies to investigate the rules developing axons use to respond to both single and multiple molecular guidance cues. This project is suitable for students with a strong biology or bioengineering background. Experience in tissue culture would be advantageous. For more details about the lab see cns.qbi.uq.edu.au.
Supervisor Dr Liviu Bodea l.bodea@uq.edu.au
Gene expression profiling in a mouse model of schizophrenia
Maternal immune activation (MIA), occurring due to infections during pregnancy, is associated with an increased risk of schizophrenia in offspring. However, it is unclear how MIA alters the foetal brain gene expression. This study examines how MIA dysregulates gene expression in the developing brain in ways relevant to schizophrenia-associated pathophysiology. Methods and techniques: qPCR, immunohistochemistry, in situ hybridization, microscopy. Students will have an opportunity to generate publications from their research. The project is suitable for students with a background or interest in neuroscience, molecular biology, and genetics.
Understanding neuronal diversity in the mammalian brain
The diversity of neuronal cells in the brain provides the basis for our complex behavioural and cognitive abilities, but how does neuronal diversity emerge and refine itself during life? Neuronal diversity can be grossly defined based on anatomical location, the shape and size of neurons, and the neurotransmitters or electrical signals sent by neurons. However, the neuronal diversity defined at the molecular level is much less understood. In recent years, the long-Interspersed Element 1 (LINE-1 or L1) retrotransposons have emerged as a novel source of DNA variation in the human brain. Through a copy-and-paste mechanism of mobilisation, L1 DNA sequences “jump” from one location in the genome to another location and alter neuronal genomes. Previous studies have demonstrated that L1 mobilisation is higher in neurons than in other brain cell types and this activity can occur during neuronal development. However, many fundamental features of L1 mobilisation during brain development are unknown. Our goal is to identify the cellular requirements and precise timing of L1 activation during neurodevelopment. The candidate for this project will learn various cell culture, immunohistochemical, microscopy, analysis of imaging data, as well as molecular biology techniques. The project is suitable for students with a background or interest in neuroscience, imaging, and molecular biology.
Systems and Computational Neuroscience
Group Leader Professor Geoffrey Goodhill g.goodhill@uq.edu.au cns.qbi.uq.edu.au
How neurons in the zebrafish brain code visual activity
We are performing experiments to determine how neurons in the zebrafish visual code information about the world, and how this neural activity is correlated with their behaviour. Projects are available in the experimental or computational aspects of this project. The experimental side is suitable for students who would like to learn state-of-the-art methods for brain imaging and/or behavioural analysis. The computational side involves advanced methods in image processing, statistical modelling and mathematical theories of neural coding, and is suitable for mathematics, physics, engineering or computer science students, particularly those with a strong programming background.
How growing nerve fibres find their targets in the developing brain
We are performing experiments to determine how growing nerve fibres find their targets in the developing brain. The experimental side is suitable for students who would like to learn state-of-the-art methods for culturing nerve cells. The computational side involves advanced methods in image processing and statistical modelling, and is suitable for mathematics, physics, engineering or computer science students, particularly those with a strong programming background.
Group Leader Dr Matilde Balbi m.balbi@uq.edu.au
Closed-loop joystick navigation for mice
Refined forelimb movements are a distinctive feature of the mammalian motor system. Goal directed limb movements allow us to perform most tasks of daily living and to manipulate objects in our environment. These highly coordinated voluntary movements integrate relevant sensory inputs and motor command. Sensorimotor integration is often disrupted in neurological disorders, such as stroke. Mice are very dexterous with their forelimbs and share many kinematics features with humans.
This project aims to:
a. Further develop a miniature robotic joystick for applying force to guide or perturb mouse forepaw movements and integrate it to our automatic system.
- Program system for applying force perturbation
- Integration of miniaturized hardware and implementation of microprocessors (Arduino, Raspberry pi)
- Program a real-time processing routine and a GUI.
b. Develop a system for high-speed videos to track and quantify forelimb movements of mice, combined with simultaneous calcium imaging recordings
- Adapt the system for online tracking and closed loop applications.
- Program a real-time processing routine and a GUI.
Requirements: strong programming background preferably in Matlab or Python will be required, highly motivated, keen interest in biology and neuroscience. We encourage applications from Aboriginal and Torres Strait Islander students, LGBTIAQ+ students and others from backgrounds underrepresented in STEMM
Ageing and Dementia Research
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Supervisor Dr Andrew Kneynsberg a.kneynsberg@uq.edu.au
Understanding the fundamental biology of microtubule associated protein tau
Alzheimer’s disease and other neurodegenerative diseases (termed tauopathies) are characterized by the accumulation of the tau protein into identifiable brain pathologies. The role of tau in disease, however, is not well understood, nor are the functions tau in healthy neurons. In order to better understand the role of tau in disease pathophysiology, our group investigates tau’s basic cellular functions. In addition to tau regulating microtubule dynamics, tau is known to play a role in axonal trafficking, phosphotransferase activity, and protein translation through interaction with Fyn kinase. These functions require specific regulation of tau localization and activity, within the intracellular compartments of neurons. The Honours candidate will investigate tau biology, localization, and involvement in cellular functions using techniques in primary cell culture, protein biochemistry, and advanced microscopy.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Supervisor Dr Liviu Bodea l.bodea@uq.edu.au
Characterisation of novel animal models generated by CRISPR technology
Our lab has a long-standing history of generating different animal models to unravel brain physiology under both healthy and pathological conditions. We have applied CRISPR-based cutting-edge genomic approaches to generate several animal models targeting different molecules important for brain function or neurodegenerative progression. The student candidate will analyse these models under the guidance of Dr. Liviu Bodea. We expect that the results from this project will have a significant impact on our understanding of how the brain functions under healthy and pathological conditions.
Group Leader Professor Fred Meunier f.meunier@uq.edu.au
How brain cells communicate and survive in health and disease
The overall goal of our research is to determine how brain cells communicate and survive in health and disease. Our lab focuses on the molecular events governing vesicular trafficking within presynaptic nerve terminals and neurosecretory cells. Our discoveries 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. In parallel to this process, internalisation of key neurotrophic factors occur at the synapse leading to survival. How these two trafficking pathways talk to each other is the focus of our current research. We have a range of projects available to honours looking at how molecular interactions govern trafficking events in synapse leading to both neurotransmission and survival.
Group Leader Dr Adam Walker adam.walker@uq.edu.au
Understanding the earliest disease mechanisms in MND and dementia
Motor neuron disease (MND) and frontotemporal dementia (FTD) are both fatal neurodegenerative diseases, which are characterised by aggregation of a protein known as TDP-43 within neurons. In screening experiments, we have identified hundreds of proteins that are altered very early in disease in genetically modified TDP-43 mice. We have several projects in which you will investigate changes in protein levels and sub-cellular localisation of several of our top-priority targets over time, in brains and spinal cords from these TDP-43 mice. You may also investigate TDP-43 aggregation and mislocalisation in cell lines and primary neurons, using CRISPR gene knockout and plasmid/lentiviral-mediated over-expression studies, and in vivo in the TDP-43 mice, using drugs and viruses. These projects will help identify the molecular mechanisms involved in TDP-43 malfunction and to understand new potential therapeutic targets for MND and FTD.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Supervisor Dr Pranesh Padmanabhan p.padmanabhan@uq.edu.au and Supervisor Dr Gerhard Leinenga g.leinenga@uq.edu.au
Understanding the dynamics of the blood-brain barrier in response to therapeutic ultrasound (2+ projects)
The brain is considered to be the last frontier, both in terms of understanding how it operates and in accessing it for therapeutic intervention. Our laboratory works in both spaces: deciphering the role of key molecules and signalling pathways in Alzheimer's disease (AD) and developing novel ultrasound-based techniques to overcome the blood-brain barrier (BBB). The BBB restricts the flow of blood-borne substances into the interstitial brain space, facilitated by tight junctions between the cells that constitute the blood vessels thereby hindering paracellular transport, and a very low number of vesicles, thereby reducing transcytosis. Application of pulsed ultrasound (US) in the presence of intravenously injected microbubbles has been shown to transiently open the BBB in different model organisms. In previous studies by our laboratory, we demonstrated that delivery of ultrasound to Alzheimer's mice mice was sufficient to remove amyloid plaques and tau tangles and restore cognitive function.
One potential Honours project study will use two-photon microscopy to investigate the dynamics of BBB opening following ultrasound treatment aided by the used of fluorescently labelled dextrans, thereby contributing to our strategies of using ultrasound as a therapy for Alzheimer's disease. Another project will use cell lines including optimized BBB in vitro systems to gain insight into the dynamics of BBB proteins in response to ultrasound.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Supervisor Dr Juan Carlos Polanco j.polanco@uq.edu.au
Elucidating how exosomal and vesicle-free tau seeds induce tau pathology in Alzheimer's Disease
Alzheimer's Disease (AD) is an irreversible and progressive dementia characterised by neurodegeneration and concomitant neuronal cell loss. The pathological progression of AD involves the aggregation and deposition of two proteins, β-amyloid, and tau. Regarding tau, a large number of studies have revealed that its pathological aggregation impairs neuronal physiology at various levels, including damage of axonal transport, action potential firing, synaptic plasticity, memory formation, nuclear transport, chromatin structure, and mitochondrial function which eventually results in neurodegeneration (Polanco et al., Nat Rev Neurol 2018). It is believed that tau pathology is induced by misfolded tau seeds that propagate transsynaptically and corrupt the proper folding of soluble tau in recipient neurons (Polanco & Götz, FEBS J 2021; Polanco et al., Acta Neuropathol Commun 2018). Tau seeds with demonstrated ability to induce tau aggregation are: (i) vesicle-free or naked tau in the form of oligomers or fibrils, and (ii) exosomal tau encapsulated by the membranes of secretory extracellular vesicles known as exosomes (Polanco et al., J Biol Chem 2016). We recently demonstrated that exosomes can deliver tau seeds into the cytosol via permeabilization of endolysosomes (Polanco et al., Acta Neuropathol 2021). My research focuses on three major lines of investigation: (i) the role of extracellular vesicles known as exosomes in the spreading and induction of Alzheimer's pathology, (ii) elucidating mechanisms by which exosomes deliver cargoes into the cytosol, and (iii) discovering genes and elucidating cellular processes that bring about tau aggregation (Briner, Götz & Polanco, Cell Rep 2020). I currently have available projects for students on the role of exosomes in AD and under physiological conditions, aiming at answering questions such as:
- Can exosomal delivery into the cytosol be controlled or modulated?
- What genes regulate exosomal delivery into the cytosol?
- How to halt or reduce tau pathology by controlling exosome production or traffic?
- What genes are important for the induction of tau aggregation?
- What’s the functional overlap between exosomal and vesicle-free tau seeds?
- How can pivotal genes for tau aggregation be regulated?
Neuroimaging
Group Leader Associate Professor Kai-Hsiang Chuang k.chuang@uq.edu.au
The laboratory aims to identify neuro-endophenotype of brain functions and disorders to improve our understanding of cognitive functions and disease processes, so as to facilitate diagnosis, prognosis and intervention. Neuroimaging, such as functional magnetic resonance imaging (fMRI), is a powerful tool that can map structural, functional and connectomic changes of the brain noninvasively. As the same technique can be applied in both humans and animals, it allows direct translation of findings in animal models to humans, or vice versa. We will use animal models to determine behaviour- or pathology-specific biomarkers and translate that to human.
Imaging brain connectome of rodent models of diseases
Neurodegenerative diseases, such as dementia, are irreversible and generally incurable and hence early detection is essential so that interventions can be applied to slow down its progression. Various diseases have been found to affect brain connectivity in disease-specific pattern, however the mechanisms are still unclear. We focused on characterising the change of brain connectome using MRI techniques for mapping structural and functional connectivity in mouse models and humans in vivo. This project will evaluate the effects of disease-associated risk genes or treatments on the brain connectome in transgenic mouse models of neurodegenerative diseases, such as Alzheimer’s disease, Huntington disease, frontotemporal dementia and amyotrophic lateral sclerosis, to improve our understanding of the genetic effects on the pathogenesis in human.
Imaging brain disorders and treatment response
Various pathogenic factors could contribute the altered neural structure and function in brain disorders. This project will identify brain disorder-related changes in patients using multimodal MRI and use them as biomarkers for assessing the treatment. In particular, we will track the structural and functional connectivity before and after the intervention and correlated with blood biomarkers and behaviour to understand the pathological effects of inflammation, amyloid plaque, cerebrovascular and metabolic dysfunction on the disease progression and the efficacy of intervention.
Understand neural basis of resting-state network
An interesting phenomenon of the brain is that certain brain areas form synchronous low frequency oscillation during the resting state. These resting-state networks can be detected by functional MRI (fMRI) noninvasively and their changes have been associated with attention, learning, memory and disorders. While widely applied, the neural basis of resting-state fMRI is largely unknown. We aim to understand the neural basis underlies the resting-state networks, the axonal connectivity that supports the network topology and their relevance to behaviour, such as learning and memory. We will apply fMRI in rodent under pharmacological and behaviour manipulations and validated by electrophysiology, neuronal tract tracing, lesion and optogenetics to determine the neural underpinning of the fMRI signal oscillation and its relationship with particular neural pathway and transmission system.
Techniques you will learn in our group may include: functional MRI, diffusion tensor imaging (DTI), image processing, neuroanatomy, brain function
Group Leader Associate Professor Margie Wright margie.wright@uq.edu.au
Our laboratory uses brain imaging (MRI: Magnetic Resonance Imaging) to study developmental brain changes that occur from late childhood into the teenage years and how changes in the brain relate to differences in cognitive and emotional functioning. Data are collected in twin pairs to assess both familial and environmental influences. In addition, we collect a broad range of phenotypes in order to examine their impact on development (including pubertal status, peer and family factors, sleep quality, early life factors, socio-economic status).
Opportunities exist for students with a background or interest in: neuroscience, magnetic resonance imaging, neuropsychology, mental health.
White Matter Microstructure in Adolescence
Adolescence represents a key period of human brain development. Studies have shown considerable changes in white matter microstructure during adolescence; however, studies have typically focused on age-related rather than puberty-related effects. Using high quality brain scans collected in a sample of young adolescents (9-12 years of age), this project aims to identify changes in white matter microstructure (e.g. fractional anisotropy, mean diffusivity) associated with pubertal stage.
Amygdala Volume and Anxiety Traits in Young Adolescents
There is a substantial literature suggesting a role for the amygdala in emotional processing, and further, amygdala vulnerability to negative environment. However, associations between amygdala volume, anxiety, and negative environmental factors, remain unclear and understudied. Adolescence is a developmental period of particular interest given adolescent vulnerability to adverse events and the increasing emergence of stress-related psychopathologies. This project will explore relationships between amygdala volume (including amygdala subfields) and anxiety traits in young adolescent twins aged 9-12 years. The effects of sex, age, and pubertal status, as well as the influence of adverse events, will be examined.
Hippocampal Volume and Cognitive Function in Young Adolescents
The hippocampus is a subcortical structure posited to mediate cognitive processes. During adolescence, maturational changes are found for both hippocampal volume and cognitive performance. This project will investigate relationships between hippocampal subfield volumes and ability on a range of cognitive traits in young adolescents aged 9-12 years. In addition to age, sex differences and the influence of pubertal stage will be explored.
Neural Circuits, Genetics and Behaviour
Group Leader Professor Barry Dickson b.dickson@uq.edu.au Dr. Kai Feng k.feng@uq.edu.au
Neural mechanisms underlying locomotion
As animals walk, run, or hop, motor circuits in the spinal cord convert descending "command" signals from the brain into the coordinated movements of many different leg muscles. How are command signals from the brain deconvolved into the appropriate patterns of motor neuron activity? We aim to answer this question for Drosophila by studying the functional organization of leg motor circuits in the ventral nerve cord, the fly’s analogue of the spinal cord. In Drosophila, individual neuronal cell types can be reproducibly identified and manipulated using genetic reagents that have been developed to target specific descending neurons, interneurons, or motor neurons. We have also established imaging pipeline to identify novel neurons that are behaviourally relevant and probe how they talk to each other. A range of projects involving optogenetics, two-photon imaging, machine learning assisted behavioural analysis and circuit modelling are currently open to honours students with a background in any area of molecular biology or experimental or theoretical neuroscience.
Group Leader Dr Zhaoyu Li zhaoyu.li@uq.edu.au
Decoding neural circuit structure and function using C. elegans as a model
Our lab ultimately seek to understand how neural network generates sensorimotor behaviour, and how dysfunction of brain network leads to behavioural deficits and disorders. Animals produce an incredible repertoire of sensorimotor behaviours to interact with the outside world. The underlying basis is synaptic connections between neurons in circuits within the nervous system. Therefore, understanding of circuit and synaptic integration and plasticity is key to decode brain functions. By employing state-of-the-art techniques such as whole brain imaging and optogenetics, we are particularly interested in 1) how neural network integrates sensorimotor information and encodes diverse behaviours, 2) how different factors such as experience, ageing and disease reshape this process. We use C. elegans, a research model with only 302 neurons to address these questions. Honours recruited in these projects not only have opportunities to address important scientific questions in this area, but also receive systematic training in neuroscience including molecular genetics, transgenic animal generation, behavioural analysis, optogenetics and imaging.
Group Leader Assoc Prof Thomas Burne t.burne@uq.edu.au Primary Supervisor Dr James Kesby j.kesby@uq.edu.au
The role of dopamine systems in reversal learning
Excess dopamine function is a key underlying factor in psychotic disorders such as schizophrenia. There is now also evidence that dopamine systems may also impair decision-making processes. Our work uses viral strategies to manipulate dopamine systems in mice performing complex decision-making tasks. Mice can be trained to perform a reversal learning task similar to that used in people with psychosis. Understanding the precise influence of excess dopamine function on reversal learning will help better understand what cognitive impairments in schizophrenia may results from excess dopamine function.
This project focusses on preclinical behavioural neuroscience and includes computational modelling to better identify underlying cognitive processes guiding behaviour.
Epigenetics, Longevity, and Molecular Biology
Group Leader Dr Steven Zuryn s.zuryn@uq.edu.au
Discovering epigenetic pathways that ensure robust cell function in during ageing and age-related diseases
When cells are faced with stress associated with ageing and disease, what rapid epigenetic response mechanisms help to preserve precise cell function? This is an especially relevant question in an age where neurodegenerative diseases are reaching epidemic proportions. We aim to identify and characterise epigenetic pathways that serve to protect cells, such as neurons and muscle cells, from the types of cellular stresses associated with disease by using powerful molecular genetic approaches in C. elegans. Because mitochondria are intimately linked with both ageing and age-related diseases, we focus on stress caused by damage to the mitochondria’s own genome.
Group Leader Dr Steven Zuryn s.zuryn@uq.edu.au
Uncovering the secrets of the mitochondria genome in C. elegans
Originating from an ancient endosymbiotic relationship, mitochondria possess their own genome – separate to the nucleus – and assume central cellular functions. How mitochondria and their genome behave in specific tissue and cellular contexts remains a challenging question in neurobiology. We have developed novel tools (published recently in Nature Cell Biology) to address this problem in the powerful genetic model organism, C. elegans. We aim to determine how quality control of the mitochondrial genome is regulated and how deregulation may lead to disease and ageing.
Functional Neuroimaging and Brain Injury
Group Leader Dr Fatima Nasrallah f.nasrallah@uq.edu.au
The relationship between traumatic brain injury and Alzheimer's disease in a transgenic mouse model
Supervisors: Dr Fatima Nasrallah and Dr Rodrigo Medeiros.
Traumatic brain injury (TBI) is considered as one of the strongest epigenetic risk factors for developing dementia, specifically Alzheimer’s disease (AD). TBI has been shown to fastforward the onset of AD by more than 4 years on average and while it is unclear the mechanism by which TBI leads to early onset of AD symptoms and sever cognitive decline, a history of moderate TBI results in a 2.3 times greater risk of developing AD while a history of severe TBI results in a 4.5 times greater risk. To understand the underlying mechanism and link between TBI and AD, we will investigate molecular and immunohistochemical markers of AD, mainly neurofibrillary tau tangles, amyloid plaques, and neuroinflammatory markers in a ALZ17 transgenic mouse model following a TBI. The study will allow us to determine the role of neuroinflammation in the process following TBI and how much that has an effect on the tau and amyloid buildup in the brain in AD. The candidate for this project will learn various immunohistochemical and molecular wet lab methods and will also have the opportunity to learn data processing of magnetic resonance imaging data that is available for these cohort of mice. If interested, please email f.nasrallah@uq.edu.au for more information.
Neuronal Degeneration and Regeneration
Group Leader Professor Massimo Hilliard m.hilliard@uq.edu.au
Group Leader Professor Massimo Hilliard m.hilliard@uq.edu.au
Identifing molecules and mechanisms of axonal degeneration
How some axons can regenerate after nerve damage while others cannot is a crucial question in neurobiology, and the answers will be of great value for the medical handling of neurodegenerative diseases and of traumatic nerve injuries. Largely unknown are the molecules and the mechanisms underlying this important biological process. In C. elegans, a new laser-based technology allows single neuron axotomy in living animals, and axonal regeneration can now be visualised in real-time and tackled with a genetic approach. Our goal is to identify the genes and conditions that control this fascinating process.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Supervisor Dr Esteban Cruz Gonzalez e.cruz@uq.edu.au
Developing therapeutic tau antibodies and understanding how they engage and clear tau
Deposition of intracellular protein aggregates of the microtubule-associated protein Tau (MAPT) are a pathogenic hallmark of a broad range of neurodegenerative disorders termed tauopathies, and are the main constituents of neurofibrillary tangles found in Alzheimer’s patients. It is now well established that patterns of tau deposition correlate well with atrophy and cognitive decline in Alzheimer’s disease (AD), pointing to the potential of developing targeted anti-Tau therapies. Among current platforms to develop targeted therapies, none match the specificity and versatility of antibodies and their derivatives, having dominated the biopharmaceutical landscape in the last two decades as a reflection of their remarkable therapeutic properties. Yet, targeting an intracellular protein like tau presents significant challenges, and several ongoing efforts in the industry have failed to provide convincing evidence of therapeutic benefit in clinical development. Our group has previously generated and characterised antibodies against tau, showing that they can ameliorate tau pathology in mouse models of tauopathy. However, the exact mechanisms through which tau antibodies exert their function is unclear, and such information is required to optimise their design. This project aims to unravel the mechanisms by which our antibodies decrease tau burden, using a combination of in vitro cell-based assays and animal models, alongside a battery of biochemical techniques to obtain a full picture of how antibodies affect relevant pathogenic processes. These insights, in conjunction with recent breakthroughs in understanding the structural properties of tau, will be harnessed to develop new optimised antibodies.
Clem Jones Centre for Ageing Dementia Research (CJCADR) under the group leadership of Professor Jürgen Götz
Dr Andrew Kneynsberg a.kneynsberg@uq.edu.au
Understanding the fundamental biology of microtubule associated protein tau
Alzheimer’s disease and other neurodegenerative diseases (termed tauopathies) are characterized by the accumulation of the tau protein into identifiable brain pathologies. The role of tau in disease, however, is not well understood, nor are the functions tau has in healthy neurons. To better understand the role of tau in pathophysiology, our group investigates tau’s basic cellular functions. In addition to tau regulating microtubule dynamics, tau is known to play diverse roles in axonal trafficking, phosphotransferase activity, and protein translation through interaction with Fyn kinase. Tau is also a scaffolding protein. These functions require a specific regulation of tau localization and activity within the different neuronal compartments. The Honours candidate will investigate tau biology, localization, and involvement in cellular functions using techniques in primary cell culture, protein biochemistry, and advanced microscopy.