Medical Research with Honours Projects and Application Guide

Why do the Bachelor of Medical Research with Honours?

Honours is a fourth-year undergraduate course where students participate in and complete a discrete research project. Honours will develop students’ skills in problem solving, planning, data analysis, reading and thinking critically, and to communicating clearly. Students will also gain project specific skills as required to complete the work. Undertaking honours gives students an example of what working as a research scientist would be like as a career, allows them to demonstrate academic excellence in an area of special interest, and provides an entry point for further research through higher degree study (i.e. PhD) and other courses.

Undertake a major research project

The critical element of the Honours program is undertaking a major research project, which involves developing research skills, conducting research, and completing a thesis detailing and discussing the findings of the project.

Add value to your resume

Investing in the additional year of study required to complete Honours gives you the opportunity to draw together your early years of study and add significant value to your resume.

Develop maturity and skills

Honours is very different from earlier undergraduate years, requiring a greater degree of independence and flexibility that will help you develop the maturity and skills for transition to employment in a range of occupations and industries or graduate research.

Student experience in honours

In your honours year, you will be directly supervised by one of our experienced researchers and their teams in your area of interest (see project information below). In addition, you will have the option of entering the Honours Mentor Program, where you will be mentored by our outstanding alumni and a current PhD student to help you overcome challenges and guide you through the honours year and research process. In addition, you will have opportunities to present your work at the annual University of Tasmania Health Research Showcase and through the Honours 3 Minute Thesis competition.

Honours projects available through the Bachelor of Medical Research with Honours

The details of research groups accepting honours students across a range of research areas are available below. Research groups offering honours projects have been grouped under three primary medical research themes. Each research theme is broad and has a range of projects that encompass discovery and laboratory research, clinical and health services research, public health and epidemiology research.

Discovery and Laboratory Research

Discovery and Laboratory research aims to fundamentally improve our understanding of biology and biological processes associated with human health and disease. Research projects generally take place in the laboratory setting and involve the use of cell culture, animal studies, tissue processing, and big data/omics techniques. Honours projects are available covering many research areas, including cancer, cardiovascular disease, obesity/type 2 diabetes, neuroscience, and many others.

Research Team: Assoc Prof Phillippa Taberlay, Dr Alex Woodworth, Dr Brandon Signal

Academic Unit:  Menzies Institute for Medical Research, Medical Science Precinct, Hobart.

Key words: epigenetics, epigenomics, chromatin structure, gene regulation

Research focus:

Our research focuses on understanding the structure and organisation of chromatin and how this influences the function of the cell. Chromatin state is tightly regulated by epigenetic factors, such as DNA methylation and histone modifications, as well as a range of chromatin modifying complexes. Together, these systems control the 2- and 3-dimensional structure of chromatin, which in turn affects the expression of genes and the identity of the cell. We are interested in how these systems function in normal cells, and how their disruption leads to cellular dysfunction and disease. To investigate this, we are developing cutting-edge techniques that allow us to examine multiple epigenetic regulatory layers at the same time. We apply these methods to answer epigenetic questions in a range of biological contexts, from cancer to neurodegeneration.

Research questions/topics:

  1. How do disruptions of chromatin modifying proteins affect the epigenome as a whole?
  2. How can we get the most epigenetic information out of limited samples?
  3. What is the contribution of the epigenome in medulloblastoma progression?
  4. How does the epigenome change as we age, and what factors affect this?
  5. How do cells respond to disruption of epigenetic regulatory systems?

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Phillippa Taberlay (phillippa.taberlay@utas.edu.au), or Alex Woodworth (morganw0@utas.edu.au) to discuss relevant honours projects available.

Key techniques:

Next-generation sequencing, PCR, cell culture, live cell imaging, chromatin immunoprecipitation (ChIP-seq), nucleosome occupancy and methylation (NOMe-seq), enzymatic methylation (EM-seq), chromatin conformation capture (HiC/microC), CUT&RUN, Cut & Tag, CRISPR, bioinformatics.

Papers of interest:

  1. Navickas, SM et al. The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target. Oncogene. 2023 Jul;42(31):2363-2373.
  2. Taberlay, PC et al. Three-dimensional disorganization of the cancer genome occurs coincident with long-range genetic and epigenetic alterations. Genome research. 2016;26(6):719-731
  3. Giles, KA et al. Integrated epigenomic analysis stratifies chromatin remodellers into distinct functional groups. Epigenetics & Chromatin. 2019;12:1-19.
Blizzard Motor Neuron Disease Research Team

Research team: Assoc Professor Catherine Blizzard

Academic Unit: Menzies Institute for Medical Research, Medical Science Precinct, Hobart.

Key words: MND, motor neuron, hyperexcitability.

Research focus:

Our team strives to unravel the complexities of altered synaptic communication in the brain and spinal cord in motor neuron disease (MND).  MND has a devastating impact on the individual diagnosed, as well as their families, and there is a desperate need for effective therapeutic interventions. We now understand that disruptions in neuronal communication may be an early and important trigger to neurodegeneration in the brain and spinal cord, and that these changes can selectively spread through the corticomotor system.

We offer a two-pronged approach to our MND research: you can either focus upon gaining critical insight into how neurodegenerative diseases start by investigating how MND spreads through the corticomotor system or you can trial new therapeutic interventions aimed at developing personalised medicine approach for MND.  Our therapeutic pre-clinical trials focus on repurposing therapies currently in practice for other diseases and delivering them in a novel and selective way, to devise an effective and targeted intervention for MND that can translate to the clinic rapidly.

Research questions/topics:

  1. Trialling transcranial magnetic therapy for MND
    Lead researcher: Assoc Prof Catherine Blizzard (Catherine.Blizzard@utas.edu.au)
  2. How does MND spread through the corticomotor system?
    Lead researcher: Assoc Prof Catherine Blizzard (Catherine.Blizzard@utas.edu.au)

We have exciting opportunities in our group for honours projects. We like to talk to potential honours candidates and then offer a project that we have funded and is also aligned to the interests of the student. We currently have funding from the NHMRC, MND Research Australia and FightMND.

Please contact Cathy (Catherine.Blizzard@utas.edu.au).

Key techniques: mouse models, cell culture, immunohistochemistry, behaviour, electrophysiology.

Papers of interest:

  1. Reale et al 2023. Pathologically mislocalised TDP-43 in upper motor neurons causes a die-forward spread of ALS-like pathogenic changes throughout the mouse corticomotor system. DOI: 10.1016/j.pneurobio.2023.102449.
  2. Handley et al., 2023. Estrogen Enhances Dendrite Spine Function and Recovers Deficits in Neuroplasticity in the prpTDP-43A315T Mouse Model of Amyotrophic Lateral Sclerosis. DOI: 10.1007/s12035-022-02742-5.
  3. Dyer et al 2021. Mislocalisation of TDP-43 to the cytoplasm causes cortical hyperexcitability and reduced excitatory neurotransmission in the motor cortex. DOI: 10.1111/jnc.15214.
Bone Marrow Failure Syndrome Group
We do a lot of work with the Hewitt lab group. Here are the two lab groups pictured together.

Research team: Dr Kirsten Fairfax

Academic Unit: Tasmanian School of Medicine, Medical Sciences Precinct, Hobart.

Keywords: Bone Marrow Failure Syndrome, haematopoiesis, genetics, immunology, bioinformatics

Research focus:

The bone marrow is like the factory for generating blood cells in the body. When the bone marrow fails individuals no longer have normal production of red blood cells, white blood cells or platelets. Our research uses different molecular biology tools, such as CRISPR and single cell sequencing to understand more about the disease. We also look at what happens in normal haematopoiesis and work towards generating new therapeutics for this devastating disease.

Research questions/topics:

  1. How do different sequences in the promoter regions of genes responsible for Bone Marrow Failure effect the function of those genes?
  2. Can we use CRISPR to make gene therapies for Bone Marrow Failure Syndromes?
  3. How does genetic variation impact blood cell formation?
  4. Can we model what goes wrong in Bone Marrow Failure Syndromes in a cell line?
  5. Can we use CRISPR screens to understand more about haematopoiesis?

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Dr Kirsten Fairfax (kirsten.fairfax@utas.edu.au) to discuss relevant honours projects available.

Key techniques: molecular biology techniques such as cloning, PCR and sequencing, flow cytometry, cell culture, biospecimen collection and handling and ELISA.

Papers of interest:

  1. S Yazar, J Alquicira-Hernandez, K Wing, A Senabouth, M Gordon, S Andersen, Q Lu, A Rowson, T Taylor, L Clarke, K Maccora, C Chen, A Cook, C Ye, Kirsten A Fairfax, A Hewitt, J Powell. Single-cell eQTL mapping identifies cell type–specific genetic control of autoimmune disease. Science 376, eabf3041 (2022).
  2. J Bolden, E Lucas, G Zhou, J O’Sullivan, C de Graaf, M McKenzie, L Di Rago, T Baldwin, J Shortt, W Alexander, B Bochner, M Ritchie, D Hilton, Kirsten A Fairfax. Identification of a Siglec-F+ granulocyte-macrophage progenitor, Journal of Leukocyte Biology, Volume 104, Issue 1, Jul 2018, Pages 123–133.
  3. J Choi, T Baldwin, M Wong, J Bolden, Kirsten A Fairfax, E Lucas, R Cole, C Biben, C Morgan, K Ramsay, A Ng, M Kauppi, L Corcoran, W Shi, N Wilson, M Wilson, W Alexander, D Hilton, C de Graaf. Haemopedia RNA-seq: a database of gene expression during haematopoiesis in mice and humans, Nucleic Acids Research, Volume 47, Issue D1, 08 January 2019, Pages D780–D785.

Research team: Dr Kelsie Raspin, Assoc Prof Liesel FitzGerald and Prof Jo Dickinson

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Keywords: cancer, familial cancer, metastatic cancer, genetics, genomics, rare variants, epigenetics, epidemiology

Research focus: Our research focusses on understanding inherited and somatic genomic changes that contribute to cancer development and its progression to metastatic disease. Family history is one of the strongest risk factors for prostate cancer and it is now clear that both common and rare genetic variants are important factors in prostate cancer development. The Tasmanian Familial Prostate Cancer Study (Topics 1 and 2) aims to identify rare genetic variants associated with prostate cancer risk and to use this knowledge to develop better screening tests.

Metastatic cancer is responsible for the majority of deaths associated with solid tumours and treatment options are mainly focused on palliative care. The Epigenetic and Molecular Determinants of Metastatic Cancer Study (Topics 2 and3) aims to identify molecular markers of cancer metastasis using real-world patient samples. This knowledge will be used as a basis for developing new or repurposing existing treatments for metastatic cancer patients.

Research topics:

  1. Analysing whole genome genetic data from Tasmanian and American prostate cancer families to identify rare prostate cancer risk variants – Assoc Prof Liesel FitzGerald (liesel.fitzgerald@utas.edu.au)
  2. Characterising the functional effect of rare prostate cancer risk variants using molecular biology techniques, including cell culture, bisulphite sequencing, and gene/protein expression assays – Assoc Prof Liesel FitzGerald  (liesel.fitzgerald@utas.edu.au) or Prof Jo Dickinson (jo.dickinson@utas.edu.au)
  3. Identifying key epigenetic drivers of cancer metastasis (prostate, breast, lung, etc.) using genome-wide methylation array and transcriptome data – Dr Kelsie Raspin (kelsie.raspin@utas.edu.au) or Prof Jo Dickinson (jo.dickinson@utas.edu.au)
  4. Functionally characterising molecular drivers of cancer metastasis using cell models and other key molecular biology techniques – Dr Kelsie Raspin (kelsie.raspin@utas.edu.au) or Prof Jo Dickinson (jo.dickinson@utas.edu.au)

There are several discrete Honours projects available in each of the above research topics. If you are interested in pursuing a project in any of these topics, please contact the relevant researcher.

Key techniques: analysing whole-genome sequencing, methylation array and transcriptome data, application of bioinformatics tools for functional prediction, candidate gene literature searches, primer design, PCR, Sanger sequencing, TaqMan genotyping, association analysis, qPCR, bisulphite sequencing and cell culture

Papers of interest:

  1. Marthick JR, Raspin K, Foley GR, Blackburn NB, Banks A, Donovan S, Malley RC, Field MA, Stanford JL, Ostrander EA, FitzGerald LM, Dickinson JL. Massively parallel sequencing in hereditary prostate cancer families reveals a rare risk variant in the DNA repair gene, RAD51C. Eur J Cancer. 2021 Dec;159:52-55.
  2. Raspin K, FitzGerald LM, Marthick JR, Field MA, Malley RC, Banks A, Donovan S, Thomson RJ, Foley GR, Stanford JL, Dickinson JL. A rare variant in EZH2 is associated with prostate cancer risk. Int J Cancer. 2021 Sep 1;149(5):1089-1099.
  3. Wilkinson EJ, Woodworth AM, Parker M, Phillips JL, Malley RC, Dickinson JL, Holloway AF. Epigenetic regulation of the ITGB4 gene in prostate cancer. Exp Cell Res. 2020 Jul 15;392(2):112055.
Cardiovascular Disease Genomics Research Group (CVDG)

Research team: Assoc Prof Phillip Melton, Prof Eric Moses

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Keywords: cardiovascular disease, metabolic syndrome, genetics of complex disease, preeclampsia, integrative omics, epigenetics, dyslipidaemia, metabolic fatty liver disease, family studies, bioinformatics, statistical genetics.

Research focus:

Advances in human genomics have demonstrated a substantial genetic component for cardiovascular disease (CVD). The primary goal of our research is to better understand the underlying genetic/epigenetic risk loci that contribute to the development of cardiovascular disease and associated risk factors. Our research primarily uses large cohort and family studies combined with whole-genome scanning methods including genome-wide association, whole-genome sequencing, epigenome-wide DNA methylation integrated with other ‘Omic level data to identify these risk susceptibility loci.

Research questions/topics:

  1. How do rare variants contribute to the genetic risk of cardiovascular disease?…
  2. Is differential DNA methylation that occurs during preeclampsia persistent and associated with increased risk of cardiovascular disease?
  3. Using machine learning for the development of poly-genomic risk scores for cardiovascular disease.
  4. What are the causal genetic loci associated with both preeclampsia and cardiovascular disease?
  5. Defining the genetic architecture of the human lipidome.

There are several discrete honours projects available in each of these research topics. If you are interested, please contact either Assoc Prof Phillip Melton (phillip.melton@utas.ed.au) or Prof Eric Moses (eric.moses@utas.edu.au) to discuss further.

Key techniques: Statistical genetics, bioinformatics, machine learning, genome-wide association studies, rare variant identification, whole-genome sequence analysis, structural variant identification, computational biology, epigenome-wide DNA Methylation studies.

Papers of interest:

  1. Cadby G, Giles G, Melton PE, Moses EK. 2022. Comprehensive genetic analysis of the human lipidome identifies loci associated with lipid homeostasis with links to coronary artery disease. Nature Communications 13(1):3124.
  2. Melton PE, Burton MA, Lillycrop KA, Godfrey KM, Rauschert S, Anderson D, Burdge GC, Mori TA, Beilin LJ, Craig JM, Olynyk JK, Holbrook JD, Pennell CE, Oddy WH, Moses EK, Adams LA, Huang RC. Epigenome-wide DNA methylation and non-alcoholic fatty liver disease in adolescence. Hepatology International. 17 (3)584-594
  3. Rauschert S, Raubenheimer K, Melton PE, Huang RC. 2020. Machine Learning and Clinical Epigenetics: Challenges for Diagnosis and Classification. Clinical Epigenetics 3;12(1):51.

Research team: Dr Liviu-Gabriel Bodea

Academic Unit: Menzies Institute for Medical Research, Medical Science Precinct, Hobart.

Keywords: microglia, brain cells communication, metabolic labelling, protein turnover, neurodegenerative diseases, cell stress, cell ageing

Research focus:

Liviu and his group are interested in how the diverse cells of the brain work together to support complex functions such as learning, memory and behaviour. We investigate which proteins are synthesised and released by cells to support brain functions, with a particular focus on microglia, the resident immune cells of the brain parenchyma. These cells not only protect against injury and infection, but also shape brain development and sustain normal function throughout life. We also explore what happens when cellular and molecular interactions fail, as occurs in neurodegenerative diseases such as Alzheimer’s, during cell stress induced by environmental or internal factors, and with ageing. By understanding these dynamic processes, we seek to uncover how the brain maintains balance and resilience, and how this knowledge can inform future treatments.

Liviu has extensive experience in guiding both undergraduate and postgraduate students into the wonders of hands-on research by fostering curiosity, creativity and scientific skills development.

Research questions/topics:

  1. How does microglial protein synthesis and release regulate neuronal function?
  2. How do microglia change from a neuroprotective to a neurotoxic state?
  3. How do protein aggregates alter microglial physiology (e.g., in Alzheimer’s disease)?
  4. How do environmental factors, such as temperature, influence microglial physiology?

We are always looking forward to welcoming new students to join our research group. There are several honours projects available on each of these research topics. If interested, please contact Liviu (liviu.bodea@utas.edu.au) to discuss.

Key techniques: cell and mouse models (including CRISPR-based generation of new models), cellular, molecular, and biochemical techniques (metabolic labelling, de novo proteomics, cloning, FACS/ fluorescence activated cell sorting, RT-PCR/real-time polymerase chain reaction, WB/western blotting), microscopy (immunostaining and image analysis, including machine learning driven).

Papers of interest:

  1. Carlisle … Bodea (STAR Protocols 2023) Three methods for examining the de novo proteome of microglia using BONCAT bioorthogonal labeling and FUNCAT click chemistry
  2. Evans, Bodea*, Götz* (eLIFE 2020) Cell-specific non-canonical amino acid labelling identifies changes in the de novo proteome during memory formation
  3. Götz, Bodea, Goedert (Nature Reviews Neuroscience 2018) Rodent models for Alzheimer disease
Eye Genetics Research Group

Research team: Kathryn Burdon, Johanna Jones.

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Keywords: Genomics, model systems, bioinformatics, variant classification

Research focus:

We study the genetic causes of inherited eye diseases and the response to treatment. We have a strong focus on childhood cataract, a rare but devastating disease which causes significant visual impairment or blindness in children. We also study more common causes of blindness in adults including keratoconus, glaucoma and ocular complications of diabetes. We do family studies to identify monogenic causes of disease and large case-control studies for complex diseases. We use genomics and bioinformatics to discover and interpret variants and use CRISPR/Cas9 gene editing in zebrafish and various cell-based assays to explore the biological effects of genes and variants. Our work informs genetic testing outcomes for inherited eye disease and furthers our understanding of the risk factors and biological pathways that contribute to blindness and treatment outcomes.

Research questions/topics:

  1. Identifying novel genes and variants that contribute to eye disease.
  2. Testing genetic variants in laboratory assays to interpret genetic test results.
  3. Using animal models to study the role of novel genes in eye disease.
  4. Using genetics to predict how patients respond to treatments for eye disease.

There are projects available in each topic, including projects that do not require lab work. Please contact Kathryn Burdon (Kathryn.Burdon@utas.edu.au), or Johanna Jones (johannaj@utas.edu.au).

Key techniques: Mendelian genetics, complex disease genetics, genome and exome sequencing, bioinformatics, variant annotation, novel gene discovery, splicing, PCR, Sanger sequencing, cell culture, zebrafish animal model, DNA and RNA, plasmids and bacteria, microscopy.

Project location: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Papers of interest:

  1. Jones JL et al. Pathogenic genetic variants identified in Australian families with paediatric cataract. BMJ Open Ophthalmol. 2022 Aug;7(1):e001064. DOI: 10.1136/bmjophth-2022-001064.
  2. Gurung RL et al. Identifying Genetic Biomarkers Predicting Response to Anti-Vascular Endothelial Growth Factor Injections in Diabetic Macular Edema Int J Mol Sci. 2022 Apr 6;23(7):4042. DOI: 10.3390/ijms23074042.
  3. Jones JL et al. A 127 kb truncating deletion of PGRMC1 is a novel cause of X-linked isolated paediatric cataract. Eur J Hum Genet. 2021 Aug;29:1206-1215 DOI: 10.1038/s41431-021-00889-8.
  4. Zhao et al. Rapid and efficient cataract gene evaluation in F0 zebrafish using CRISPR-Cas9 ribonucleoprotein complexes. Methods 2021 19437-47. DOI: 10.1016/j.ymeth.2020.12.004.

Research team: Dr Jessica Fletcher

Academic Unit: Menzies Institute for Medical Research, Medical Science Precinct, Hobart.

Key words: Glial cells, oligodendrocytes, oligodendrocyte progenitor cells, microglia, multiple sclerosis, myelin repair, neuroinflammation, intracellular signalling.

Research focus:

Glial cells are the non-neuronal cells of the brain. Glial cells are the non-neuronal cells of the brain. They are critically important for maintaining brain health and supporting and protecting nerve cells. Our group is interested in how glial cells communicate with each other (and neurons) and how this communication affects their behaviour and function. Our goal is to use the knowledge generated through our research to develop new therapeutic strategies to treat brain disease. Our primary disease focus is Multiple Sclerosis, and we are part of the MS Research Flagship at the Menzies.

Research questions/topics:

  1. How does ageing change the way the brain responds to myelin damage? Research Team: Dr Jessica Fletcher
  2. Why do immature oligodendrocytes eat brain connections? Research Team: Dr Jessica Fletcher, Jia Yi Hoe
  3. Why does myelin repair fail in people with Multiple Sclerosis? Research Team: Dr Jessica Fletcher, Annalisa Pozzacchio
  4. What are the molecules that cause neuron injury after myelin damage? Research Team: Dr Jessica Fletcher

There are honours projects available across each of these research topics. If you are interested, please contact Dr Jessica Fletcher (jessica.fletcher@utas.edu.au) to discuss projects available.

Key techniques:

Literature review, fluorescence microscopy, immunohistochemistry, histopathology, image analysis, transgenic animal models, transcriptomics, cell culture, protein biochemistry, western blotting. Projects may include wet-lab experiments, microscopy and image analysis, and/or analysis of transcriptomic datasets, depending on student interests and project availability.

Papers of interest:

  1. Nicholson M, Wood RJ, Murray SS, Fletcher JL. 2026. Neuronal TrkB supports adult cortical oligodendrogenesis in the brains of older adult mice. Neurobiology of Aging. 10.1016/j.neurobiolaging.2025.12.009
  2. Fletcher JL*, Makowiecki K*, Cullen CL, Young KM. 2021. Oligodendrogenesis and myelination regulate cortical development and circuit function. Seminars in Cell & Developmental Biology, 10.1016/j.semcdb.2021.03.017.
  3. Nguyen HTH, Wood RJ, Prawdiuk AR, Furness SGB, Xiao J, Murray SS, Fletcher JL. 2019. TrkB agonist LM22A-4 increases oligodendroglial populations during myelin repair in the corpus callosum. Frontiers in Molecular Neuroscience, 10.3389/fnmol.2019.00205.
The Glial Research Team

Research team: Prof Kaylene Young

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Key words: Oligodendrocytes, astrocytes, microglia, multiple sclerosis, myelination, demyelination, brain repair.

Research focus:

Our team undertakes research spanning basic neuroscience, preclinical multiple sclerosis research and clinical trials. A key area of interest is uncovering the molecular and cellular mechanism that allow newborn and existing oligodendrocytes to support lifelong learning. Another is identifying the signalling pathways and cell types that drive multiple sclerosis pathology, to help develop treatments that protect and/or repair the brain.

Research questions/topics:

To enquire about honours projects offered by the Glial Research Team, please contact Prof Kaylene Young (Kaylene.young@utas.edu.au). Potential research topics include:

  1. Do oligodendrocytes adapt to support learning in the aged brain?
  2. How does myelin loss alter neuronal communication?
  3. How do gene variants make the brain more susceptible to multiple sclerosis pathology?
  4. What do oligodendrocyte progenitor cells do in the mature brain?
  5. How can we change the brain environment to promote myelin repair?

Key techniques: Transgenic and CRISPR modified mice; human induced pluripotent stem cell culture; immunohistochemistry; fluorescence confocal microscopy; super-resolution confocal microscopy; time-lapse microscopy; image analysis; RNA sequencing; 2photon imaging; learning paradigms and behavioral studies.

Papers of interest:

  1. Zhen Y, Cullen CL, Ricci R, Summers BS, Rehman S, Ahmed ZM, Foster AY, Emery B, Gasperini R, Young KM (2022). Protocadherin 15 suppresses oligodendrocyte progenitor cell proliferation and promotes motility through distinct signalling pathways. Commun Biol. 5(1):511. DOI: 10.1038/s42003-022-03470-1.
  2. Cullen CL, Pepper RE, Clutterbuck MT, Pitman KA, Oorschot V, Auderset L, Tang AD, Ramm G, Emery B, Rodger J, Jolivet RB, Young KM (2021). Periaxonal and nodal plasticities modulate action potential conduction in the adult mouse brain. Cell Rep. 34(3):108641. DOI: 10.1016/j.celrep.2020.108641.
  3. Fortune AJ, Fletcher JL, Blackburn NB, Young KM (2022). Using MS induced pluripotent stem cells to investigate MS aetiology. Mult Scler Relat Disord. 63:103839. DOI: 10.1016/j.msard.2022.103839.

Research team: Dr Gary Morris

Key words: Microglia, astrocytes, pericytes, endothelial cells, blood-brain-barrier, Alzheimer’s disease, glymphatics cerebral amyloid angiopathy, neuroinflammation.

Research focus:

Non-neuronal cells residing within the brain, including astrocytes and microglia, closely associate with the brain vasculature to form the Gliovascular Unit. We aim to understand the physiological functions of the gliovascular unit, which we hypothesise influences the control of brain blood flow, blood-brain-barrier protection and brain waste removal. We investigate how these healthy interactions break down and contribute to microvascular dysfunction in neurological conditions, with a focus on Alzheimer’s disease dementia. We work closely with the Perivascular Research Group led by A/Prof. Brad Sutherland and the Microglia in Neurological Diseases group led by A/Prof. Jenna Ziebell.

Research questions/topics:

  1. How does the spatial relationship between microglia, astrocytes and brain blood vessels change across the spectrum of human Alzheimer’s disease dementia?
  2. What is the ultrastructural relationship between glia and the brain vasculature in health and in Alzheimer’s disease dementia?
  3. Do microglia contribute to dysfunction of the brain vasculature in Alzheimer’s disease?
  4. What molecular mechanisms do microglia use to process and deposit waste around the brain vasculature?
  5. Do microglia contribute to brain waste removal via the glymphatic system?

There are discrete honours projects available across these research topics. If you are interested, please contact Dr Morris (gary.morris@utas.edu.au) to discuss relevant honours projects available.

Key techniques: Multiplex fluorescent immunohistochemistry, fluorescent and brightfield microscopy (slide scanning, confocal, two-photon), histopathology, image analysis (including electron microscopy image analysis), transgenic animal models, biochemical assays.

Project location: Wicking Dementia Research and Education Centre, Medical Sciences Precinct, Hobart.

Papers of interest:

  1. Morris et al., (2024) Microglia contact cerebral vasculature through gaps between astrocyte endfeet. Journal of Cerebral Blood Flow and Metabolism; 44(12):1472-1486.
  2. Morris et al., (2023) Microglia directly associate with pericytes in the central nervous system. Glia;71(8):1847-69.
  3. Courtney et al., (2021) An Automated Approach to Improve the Quantification of Pericytes and Microglia in Whole Mouse Brain Sections. eNeuro;8(6).

Research team: Professor Jo Dickinson, Dr Kelsie Raspin, Dr Sionne Lucas, Dr Ella Smalley and Dr Kath Southam

Academic Unit: Menzies Institute for Medical Research, Medical Science Precinct, Hobart.

Key words:  idiopathic pulmonary fibrosis, familial interstitial lung disease, telomere biology disorder, genetics, genomics, family studies, rare variant identification, novel gene discovery, functional assays, bioinformatics.

Research focus: Interstitial lung diseases are a group of rare diseases of which pulmonary fibrosis (PF) is the most commonly diagnosed. PF is progressive and fatal with a life expectancy of 2-5 years following diagnosis, which is poorer than most cancers. Further there are limited effective treatments, and lung transplant remains the only option. It is now known that genetics plays a major role in driving the development of this disease with relatives of those diagnosed with PF at >100 times increased risk of developing disease compared with those with no family history. Rare genetic changes in several key cellular pathways are implicated in driving the disease process leading to progressive fibrosis and increasing lung damage. These pathways include those controlling telomere biology and genome stability in the cell, the production of lung surfactants, and lung cell signalling pathways. In addition, it is known that environmental factors such as smoking, and air pollutants interact with these genetic factors to worsen disease.

Our team has established a nation-wide genetic study recruiting individuals with PF and their family members with the aim of identifying the genetic cause of disease through genomic analysis. Further we propose to define how these genetic changes contribute to the pathogenetic pathways contributing to PF. To do this we utilise a variety of laboratory based cellular and molecular approaches. This research program offers great promise in terms of aiding early diagnosis and discovery of targeted treatments for PF.

Research questions/topics:

  1. How do the genetic changes we identify impact gene function in the cell and then how does this then cause disease?
  2. How do genetic changes in telomere biology genes affect telomere length and how does this impact lung cell function?
  3. How do genetic changes in the different cellular pathways interact with environmental factors to drive pathogenic processes in the lung?

There are several honours projects available across these research topics. If you are interested, please contact Prof Jo Dickinson (jo.dickinson@utas.edu.au) or Dr Kelsie Raspin (Kelsie.raspin@utas.edu.au) or Dr Ella Smalley (ella.smalley@utas.edu.au).

Key techniques: genome sequencing, bioinformatics, transcriptomics, variant annotation, cell culture, DNA sequencing, molecular biology techniques, immunohistochemistry, microscopy.

Papers of interest:

  1. Lucas SEM, Raspin K, Mackintosh J, et al. Preclinical interstitial lung disease in relatives of familial pulmonary fibrosis patients. Pulmonology. 2022.
  2. Nelson N, Feurstein S, Niaz A, et al. Functional genomics for curation of variants in telomere biology disorder associated genes: A systematic review. Genetics in medicine: official journal of the American College of Medical Genetics. 2022;25(3):100354.
Metabolism and Vascular Research Group (MVRG)

Research team: Dr Dino Premilovac, Assoc Prof Renee Ross

Academic Unit: Tasmanian School of Medicine, Medical Sciences Precinct, Hobart.

Keywords: physiology, microvasculature, blood flow, obesity, type 2 diabetes, metabolism, pharmacology,  exercise, cardiovascular disease, stroke, retinopathy, neuropathy

Research focus: The primary goal of our research is to better understand the relationship between blood flow and metabolism in organs such as skeletal muscle, adipose tissue and the brain. To do this, we study how blood flow and metabolism are linked in health to enable normal function and how these processes are altered in disease states including obesity, type 2 diabetes, ischaemic stroke, dementia, diabetic retinopathy, and peripheral neuropathy. Our research group has run honours projects for many years and we primarily use animal models to investigate the complex interplay between blood vessels and metabolism in health and disease. We are experts in many techniques including real-time blood flow imaging using ultrasound, biochemistry, pharmacology, anatomical assessment using histology and microscopy, as well as sophisticated methods for assessment of metabolism such as glucose tolerance testing, radioactive glucose tracing and the insulin clamp technique.

Research questions/topics:

  1. Developing novel ways to reduce brain damage after a stroke. Lead researcher: Dino
  2. Can we use ultrasound deliver drugs specifically to the brain?  Lead researcher: Dino
  3. Using ultrasound to quantify brain blood flow changes in health and disease. Lead researcher: Dino
  4. Can insulin and GLP1 (Ozempic) be used to prevent cognitive decline in obesity and type 2 diabetes? Lead researcher: Dino
  5. How is skeletal muscle blood flow controlled in health and exercise, and how does this change in obesity and type 2 diabetes? Researchers: Dino and Renee

There are several discrete honours projects available in each of these research areas. If you are interested, please contact Dr Dino Premilovac (Dino.Premilovac@utas.edu.au) or Assoc Professor Renee Ross (Renee.Ross@utas.edu.au) to discuss further.

Key techniques: animal models of disease, microsurgical techniques for in vivo experiments, exercise testing, ultrasound for blood flow imaging, ultrasound for drug delivery, metabolic profiling including use of radioactive glucose isotopes, histology, immunohistochemistry, and microscopy.

Papers of interest:

  1. Southam K, de Sousa C, Daniel A, Taylor BV, Foa L, Premilovac D. Development and characterisation of a rat model that exhibits both metabolic dysfunction and neurodegeneration seen in type 2 diabetes. The Journal of Physiology. 2022 Apr;600(7):1611-30.
  2. Premilovac D, Blackwood SJ, Ramsay CJ, Keske MA, Howells DW, Sutherland BA. Transcranial contrast-enhanced ultrasound in the rat brain reveals substantial hyperperfusion acutely post-stroke. Journal of Cerebral Blood Flow and Metabolism. 2020 May;40(5):939-53.
  3. Attrill E, Richards SM, Ross RM, Sutherland BA, Premilovac D. Induction of Type 2 Diabetes in Mice to Understand Vascular Changes That Drive Diabetic Retinopathy. Diabetic Retinopathy: Methods and Protocols 2023 Jun 17 (pp. 1-12). New York, NY: Springer US.
Metabolic Health Group

Research team: Dr Darren Henstridge, Dr Stephen Myers.

Academic Unit: School of Health Sciences, Launceston.

Key words: Obesity, type 2 diabetes, insulin resistance, skeletal muscle, fatty liver, mitochondria, exercise.

Research focus:

Dr Henstridge’s research focuses on using pre-clinical and/or cellular models of insulin resistance, type 2 diabetes, obesity and fatty liver to study metabolic phenotypes, pathways and processes. His research is primarily focused on understanding mitochondrial and whole-body metabolic dysfunction and identifying genetic or pharmacological targets to treat these conditions.

Research questions/topics:

  1. How does altering mitochondrial function in skeletal muscle alter metabolism?
  2. Is the mitochondria a therapeutic target in fatty liver disease?
  3. How does the diabetes drug metformin actually work?

There are discrete honours projects available within these general research topics. If you are interested, please contact Dr Darren Henstridge (darren.henstridge@utas.edu.au) to discuss relevant honours projects available.

Key techniques: animal models of disease, metabolic phenotyping, cell culture models, viral vectors, western blotting, qPCR, ELISA.

Project location: The Shed Building, Inveresk, Launceston, University of Tasmania.

Papers of interest:

  1. ACAD10 is not required for metformin's metabolic actions or for maintenance of whole-body metabolism in C57BL/6J mice. Yew MJ, Heywood SE, Ng J, West OM, Pal M, Kueh A, Lancaster GI, Myers S, Yang C, Liu Y, Reibe S, Mellett NA, Meikle PJ, Febbraio MA, Greening DW, Drew BG, Henstridge DC. Diabetes Obesity & Metabolism. 2024 May;26(5):1731-1745.
  2. King EJ, Bond ST, Yang C, Liu Y, Calkin AC, Henstridge DC*, Drew BG*. Loss of Trim28 in muscle alters mitochondrial signalling but not systemic metabolism. Journal of Endocrinology. 2023 Oct 9;259(2):e230210.
  3. Zoll J, Read MN, Heywood SE, Estevez E, Marshall JPS, Kammoun HL, Allen TL, Holmes AJ, Febbraio MA, Henstridge DC. Fecal microbiota transplantation from high caloric-fed donors alters glucose metabolism in recipient mice, independently of adiposity or exercise status.
    American Journal of Physiology: Endocrinology & Metabolism. 2020 Jul 1;319(1):E203-E216.
Microglia in Neurological Diseases

Research team: Jenna Ziebell

Academic Unit: Wicking Dementia Research and Education Centre, Medical Sciences Precinct, Hobart.

Key words: neuroscience, microglia, dementia, traumatic brain injury, neurodegeneration

Research focus:

Our group’s interests include experimental models of neurological disease including traumatic brain injury and dementia. The research primarily focuses on the inflammatory cascades initiated in these diseases and how this influences disease progression, neuronal circuits, as well as cognition and motor function.

Research questions/topics:

  1. Microglia: does their role in synaptic remodeling change with age?
  2. How do microglia:synapse dynamics change with Alzheimer’s disease?
  3. Are microglia drivers of Alzheimer's disease?
  4. How do microglia contribute to obesity, insulin resistance and type 2 diabetes?
  5. Role of gliosis (microglial and astrocytic) in traumatic brain injury

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Jenna (Jenna.ziebell@utas.edu.au) to discuss relevant honours projects available.

Key techniques: animal models, immunohistochemistry, image analysis, rodent models of neurodegeneration, behaviour

Papers of interest:

  1. Doust YV, Bindoff A, Holloway OG, Wilson R, King AE, Ziebell JM (2022). Temporal changes in the microglial proteome of male and female mice after a diffuse brain injury using label-free quantitative proteomics. Glia1-24
  2. Langley RC, Canty AJ, Ziebell (2023). Repeated Measurement of Microglia‐Dendritic Spine Interactions Using Multi‐Photon Imaging, Current Protocols3(5):e791
  3. Holloway OG, King AE, Ziebell JM (2020). Microglia demonstrate local mixed inflammation and a defined morphological shift in an APP/PS1 mouse model. Journal of Alzheimer's Disease77(4):1765-1781

Research team: Dr Gabriela Bodea

Academic Unit: Tasmanian School of Medicine, Medical Sciences Precinct, Hobart.

Key words: molecular and cellular neuroscience, neurogenetics, retrotransposons, neurodevelopment, neurodegeneration

Research focus:

Genes and environment interact in complex ways to generate the remarkable diversity of brain cells that underpin our ability to respond and adapt to various stimuli. Our research aims to dissect these mechanisms to better define neuronal diversity and understand brain plasticity. We also aim to determine the intrinsic and extrinsic factors that contribute to why certain neuronal subtypes are more vulnerable to disease than others. Specifically, we investigate the role of retrotransposons. These are a type of repetitive, mobile DNA sequences that are highly responsive to environmental factors and can influence gene expression through various mechanisms. Our research seeks to understand how retrotransposons mediate gene-environment interactions in neurons, particularly in the context of brain plasticity and adaptation, and its implications for neuropsychiatric and neurodegenerative diseases.

Research questions/topics:

  1. What mechanisms regulate retrotransposon transcription in brain cells?
  2. How are retrotransposons co-opted as regulatory elements to control transcription of essential protein-coding genes in neurons?
  3. How do retrotransposons influence neuronal differentiation during brain development?
  4. How do retrotransposons respond in maternal immune activation models of psychiatric disease?
  5. How and when are retrotransposons activated in neurodegenerative conditions?
  6. How does neurotropic viral infection affect retrotransposon expression, and what are the long-term consequences for brain physiology?

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Dr Gabriela Bodea (gobodea@utas.edu.au) to discuss further.

Key techniques: RNA fluorescence in situ hybridization, confocal microscopy, image analysis, shRNA and CRISPR/dCas9-based gene expression modulation, long-read DNA sequencing, transcriptomics, cultured cells, animal models of disease.

Papers of interest:

  1. Bodea GO, Botto JM, Ferreiro ME, Sanchez-Luque FJ, de Los Rios Barreda et al. LINE-1 retrotransposons contribute to mouse PV interneuron development. Nat Neurosci. 2024 Jul;27(7):1274-1284. DOI: 10.1038/s41593-024-01650-2.
  2. Bodea GO, McKelvey EGZ, Faulkner GJ. Retrotransposon-induced mosaicism in the neural genome. Open Biol. 2018 Jul;8(7):180074. DOI: 10.1098/rsob.180074.

Research team: Dr Bennet McComish, Dr Nicholas Blackburn

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Keywords: genomics, computational, multiple sclerosis, gene expression, genetic associations, rare variants, DNA sequencing

Research focus:

Multiple sclerosis (MS) is a life destroying neurological condition that begins in early adulthood resulting in progressive neurological degeneration, disability, and eventual death. Family history is a significant risk factor for MS and there is an established genetic component to this disease. Case-control genome-wide association studies have identified over 200 regions in the genome that are associated with the development of MS, but these associations have led to very few confirmed MS risk genes. Our research uses computational genomic techniques to identify and understand MS risk genes. The McComish group uses an evolutionary medicine approach, identifying MS risk variants that have been the subject of natural selection in the population and investigating how these interact with other variants in case–control data. In the Blackburn group this is via studying multi-case MS families to identify rare genetic variants shared by affected family members, and analysing data from in vivo and in vitro models of these variants.

Research questions/topics:

  1. Does rare genetic variation contribute to the development of both MS and autoimmune diseases in a single family? (Blackburn)
  2. Do rare genetic variants identified in families with MS impact gene expression? (Blackburn)
  3. How has natural selection shaped geographical patterns of MS prevalence? (McComish)
  4. Identifying evolutionary trade-offs that have driven autoimmune disease risk. (McComish)

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Dr Nicholas Blackburn (Nicholas.Blackburn@utas.edu.au) or Dr Bennet McComish (Bennet.Mccomish@utas.edu.au) to discuss relevant honours projects available. Our projects are predominantly analytical in scope so will interest students who have a desire to work in a computational space.

Key techniques: genome sequencing, bioinformatics, transcriptomics, variant annotation, population genetics, landscape genomics

Papers of interest:

  1. Fortune AJ, Fletcher JL, Blackburn NB, Young KM (2022) Using MS induced pluripotent stem cells to investigate MS aetiology. Mult Scler Relat Disord 63:103839
  2. Fortune AJ, Taylor BV, Charlesworth JC, Burdon KP, Blackburn NB, Fletcher JL, Mehta A, Young KM (2022) Generation and characterisation of four multiple sclerosis iPSC lines from a single family. Stem Cell Res 62:102828
Neurodegenerative Disease Research Group

Research team: Dr Rachel Atkinson, Dr Andrew Phipps, Professor Anna King

Academic Unit: Wicking Dementia Research and Education Centre, Medical Sciences Precinct, Hobart

Key words: Motor neuron disease (MND), Alzheimer’s disease, dementia, neuroscience, animal/cell models, human tissue.

Research focus:

Our research team is part of the Wicking Dementia Research and Education Centre. We focus on understanding, preventing, and treating neurodegenerative diseases such as motor neuron disease, frontotemporal dementia and Alzheimer's disease. Using cell culture models, and tissue from human and animal disease models, we aim to understand the degeneration of nerve cells, why certain cells are more vulnerable to disease, and how we can protect them. Our work is collaborative and innovative, with the ultimate goal of improving the lives of people affected by neurodegenerative diseases and providing better treatments for them.

Currently, we are focusing on two research topics. The first research strategy involves utilising natural protective mechanisms found in nature to help treat diseases like motor neuron disease. The second topic aims to characterise the molecular changes occurring to the long, vulnerable motor neuron fibres that connect our neurons to our muscles, and to identify new targets for therapeutic intervention.

Research questions/topics:

Our overarching aim is to find new targets to protect the brain and prevent the neurodegeneration which leads to the symptoms of these diseases such as memory loss, loss of cognitive function and loss of movement.

Example research questions/topics:

  1. Can we harness hypothermia to treat neurodegenerative disease? Lead Researcher: Dr Rachel Atkinson (Rachel.Atkinson@utas.edu.au)
  2. Using bioinformatic approaches to identify therapeutic targets in Motor Neuron Disease. Lead Researcher: Dr Andrew Phipps (Andrew.Phipps@utas.edu.au)
  3. Understanding axon degeneration in Motor Neuron Disease with iPSCs & human MND cases. Lead Researcher: Dr Andrew Phipps (Andrew.Phipps@utas.edu.au)

We are looking forward to welcoming new students to join our research team. There are several distinct honours projects available in each of these research topics. If you are interested, please contact the researcher noted so that we can meet to discuss the relevant projects available.

Key techniques: Cell culture, live imaging (in vivo and in vitro) and cell tracing, working with animal models, biochemistry (proteomics, western blotting, ELISA), proteomics, transcriptomics, histology, immunohistochemistry, microscopy, epigenetics, bioinformatics.

Papers of interest:

  1. Collins JM, Atkinson RAK et al. Neurobiol Dis, 2022. 172: p. 105821.
  2. Phipps AJ, Dwyer S et al., Heliyon. 2024 Jul 14;10(14):e34587. DOI: 10.1016/j.heliyon.2024.e34587
  3. Signal, B., Phipps, A. J., et al., (2024). Cells, 13(16), 1393. DOI: https://doi.org/10.3390/cells13161393
Neuroepigenetics (Marshall Group)

Research team: Dr Owen Marshall (owen.marshall@utas.edu.au)

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Key words: Epigenetics, neuroscience, brain cancer, brain development, Alzheimer’s disease, gene transcription

Research focus:

Our research aims to understand the transcriptional and epigenetic changes that drive brain development and disease. We are particularly interested in how chromatin and transcription factors combine to control cell fate. Our research uses cutting-edge molecular, behavioural and imaging techniques to uncover how the brain develops, how the brain responds to ageing, and how epigenetics and gene regulation are disrupted in diseases such as Alzheimer's disease and the intractable and deadly brain cancer, glioblastoma. Our lab website has more details about what we do.

Research questions/topics:

  1. How do transcription factors and chromatin control the fate of stem cells in the brain?
  2. What are the molecular and epigenetic changes driving brain cancer?
  3. How does gene transcription in neurons change during Alzheimer’s disease and ageing?

There are several honours projects available in each of these research topics and related areas. If you’re interested in what we do, please contact Owen to discuss potential research projects.

Key techniques: Animal (Drosophila) behaviour Immunohistochemistry and confocal microscopy Next-generation sequencing and data analysis Molecular biology and cloning

Papers of interest:

  1. Delandre C, McMullen JPD, Paulsen J, Collas P & Marshall OJ. Eight principal chromatin states functionally segregate the fly genome into developmental and housekeeping roles. biorXiv. DOI: 10.1101/2022.10.30.514435
  2. Veen K, Nguyen P-K, Froldi F, Dong Q, Alvarez‐Ochoa E, Harvey KF, McMullen JPD, Marshall OJ, Jusuf PR, Cheng LY. (2023) Dedifferentiation‐derived neural stem cells exhibit perturbed temporal progression. EMBO Reports, e55837.
  3. Delandre C and Marshall OJ. (2019) United colours of chromatin? Developmental genome organisation in flies. Biochemical Society Transactions. BST20180605.

Research team: Dr John Lin, Dr Andrew Reading, Dr Agnieszka Zbela

Academic Unit: Tasmanian School of Medicine, Medical Sciences Precinct, Hobart.

Key words: protein engineering, optogenetics, neuroscience, neurophysiology, optical techniques, instrumentation

Research focus:

Important research isn't limited to projects with direct relevance diseases or its models. Technological breakthroughs, for instance, can usher in novel approaches for studying biology, enhance model development, expedite scientists' ability to tackle intricate biological inquiries, and even harbor the potential for commercial success. Optogenetics is a potent approach that utilises protein-based tools, in conjunction with optical control, to manipulate biological functions. Our research focuses on developing new protein-based tools for neuroscientific researchers to manipulate various neuronal functions including intracellular biochemical signaling, neurotransmitter release and membrane excitability. We design novel recombinant proteins using protein engineering approaches and develop novel cell-based assay to assay and validate the designs. Our projects are suitable for students that desire to have intellectual challenges and cutting edge explorational scientific questions.

Research questions/topics:

  1. Design and testing of a reversible vesicle specific optogenetic inhibitor of neurotransmitter release system.
  2. Targeting of novel optogenetic G protein inhibition system to Mu opioid receptor using receptor active-state specific nanobody.
  3. Development of antibody-mimetic protein domains to bring optogenetics to endogenous proteins.
  4. Optogenetic and sonogenetic manipulation of membrane excitability with hTRPA1 channel.
  5. Development of novel potassium-selective channelrhodopsin variants for improved kinetic control of membrane excitability.

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Dr. John Y. Lin (john.lin@utas.edu.au), to discuss relevant honours projects available.

Key techniques: Molecular cloning, cellular optical imaging, electrophysiology and assay development

Papers of interest:

  1. Lockyer J et al. (2023). Optogenetic inhibition of Gα signaling alters and regulates circuit functionality and early circuit formation. bioRXiv: 10.1101/2023.05.06.539674v1
  2. Mermet-Joret N. et al. (2021). Dual-color optical activation and suppression of neurons with high temporal precision. bioRXiv: 10.1101/2021.05.05.442824v1
  3. Lin JY et al. (2013). Optogenetic inhibition of synaptic release with chromophore-assisted light inactivation (CALI). Neuron 79: 241-253.
Perivascular Research Group

Research team: Prof Brad Sutherland, Dr Hannah Coombe

Academic Unit: Tasmanian School of Medicine, Medical Sciences Precinct, Hobart.

Key words: Neuroscience, cerebral blood flow, pericytes, stroke, Alzheimer's disease.

Research focus:

For brain tissue cells (e.g. neurons) to function, they require energy which is supplied by the vascular system, but the mechanisms that control this locally are complex. Our group uses laboratory-based techniques to understand how the vascular system provides energy to support the function of the brain and other organs (e.g. skeletal muscle and placenta), and how this becomes dysfunctional in disease. Specifically, our group focuses on a cell on capillaries called pericytes, which regulate capillary blood flow. We are interested in how pericytes function, how they communicate between the tissue and blood vessels, the signalling pathways controlling this, and how these processes go wrong in diseases such as stroke and Alzheimer’s disease.

Research questions/topics:

  1. Are pericytes responsible for acute blood flow deficits and long-term recovery following ischaemic stroke?
  2. How do pericytes interact with other cells to maintain vascular function?
  3. Are pericytes implicated in neurovascular dysfunction in Alzheimer’s disease and cerebral amyloid angiopathy?
  4. Is impaired capillary growth and pericyte coverage responsible for foetal growth restriction in the placenta?

There are several discrete honours projects available on each of these research topics. If you are interested, please contact Prof Brad Sutherland (brad.sutherland@utas.edu.au) to discuss further.

Key techniques: Immunohistochemistry, microscopy (slide scanning, confocal, two-photon), western blotting, cell culture, biochemical assays, proteomics, transcriptomics, qPCR, pharmacology, animal models of disease.

Papers of interest:

  1. King et al., (2024) Induced pluripotent stem cell derived pericytes respond to mediators of proliferation and contractility. Stem Cell Research & Therapy 15 (1), 59.
  2. Morris et al., (2023) Microglia directly associate with pericytes in the central nervous system. Glia;71(8):1847-69
  3. Brown et al., (2023) Brain pericytes in culture display diverse morphological and functional phenotypes. Cell Biol Toxicol
  4. Courtney et al., (2021) An Automated Approach to Improve the Quantification of Pericytes and Microglia in Whole Mouse Brain Sections. eNeuro;8(6)

Find out more at the Perivascular Research Group website

Stem Cell Models Group

Research team: Assoc Prof Tony Cook, Dr Bryony Thorne, Dr Emma Wilkinson.

Academic Unit: Wicking Dementia Research and Education Centre, Medical Science Precinct, Hobart.

Key words: Induced pluripotent stem cells, neurodegenerative disease, high-content imaging.
Research focus: Our group uses iPSC to better understand mechanisms contributing to neurodegenerative diseases, and to test novel therapeutic strategies. Current major projects include:

  1. Understanding gene x environment interactions that increase risk for amyotrophic lateral sclerosis (ALS). There are many genetic and environmental factors that may increase an individual’s risk of developing ALS, however, the ways in which these factors interact to cause disease are poorly understood. We are using CRISPR/Cas-edited iPSC models to explore an array of these potential interactions and whether they promote neurodegeneration.
  2. Childhood dementia caused by lysosomal storage disorders (LSDs) that result in accumulation of glycosphingolipids (GSLs). Accumulation of the lipids can be limited using drugs that are analogues of D-glucose, but these typically have a poor side effect profile (chronic diarrhea, tremor). We have designed a novel antisense oligonucleotide (ASO), an emerging class of highly specific therapeutic, that we hypothesize will limit GSL accumulation and overcome these limitations. We are now testing efficacy of this ASO in iPSC models of LSDs that cause childhood dementia.

Research topics:

  1. Are neurons with ALS-associated genetic risk more vulnerable to environmental pesticides? Lead researcher: Dr Bryony Thorne (bryony.thorne@utas.edu.au)
  2. Can UGCG-targeting ASOs limit glycosphingolipid accumulation and prevent neurodegeneration in childhood dementia?
    Lead researcher: Dr Emma Wilkinson (ej.wilkinson@utas.edu.au)

There are several honours projects available in each of these topics. If you are interested, please contact the specific researcher noted to discuss relevant honours projects available.

Key techniques: induced pluripotent stem cell culture and differentiation to brain and vascular cell types, high-content image analysis, immunocytochemistry, CRISPR editing, electrophysiology, ‘omics technologies.

Papers of interest:

  1. Chear et al. Lysosomal alterations and decreased electrophysiological activity in CLN3 disease patient-derived cortical neurons. Dis Model Mech (2022) 15 (12): DOI: 10.1242/dmm.049651

Research team: Dr William Reay

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart.

Keywords: Genetics, drug repurposing, drug discovery, precision medicine, bioinformatics, nutritional biochemistry, mental health, schizophrenia, cardiovascular disease, neurological disorders, respiratory disease, comorbidities

Research focus:

Common, complex disorders (e.g., heart disease, asthma, mental health conditions etc.) remain the largest burden on the Australian health system. A hallmark of these disorders is heterogeneity, with complex underlying biology and immense variability between individuals with the same diagnosis. Studying genetic risk for these disorders offers an unprecedented opportunity to better understand these sources of heterogeneity and influence clinical practice. The primary goal of our research is to accelerate the translation of genomics to inform prevention and treatment of these common, chronic disorders. We use large-scale genomics datasets to identify the aspects of genetic risk for these disorders that may be targets for treatment through either pharmacological intervention or lifestyle modification. We collaborate with a diverse range of scientists and clinicians both nationally and internationally to achieve these goals.

Research questions/topics:

  1. How can we use genetics to identify treatment targets for complex disorders, e.g., brain disorders?
  2. Can we leverage genomics to better predict response to treatments and adverse side effects?
  3. What is the influence of genetics on the metabolism and function of nutrients?
  4. What is the biological link between diseases that disproportionately are diagnosed together, e.g., mental health and heart disease? Are there implications of this for clinical management?
  5. Is there a role for genomics in clinical practice for risk stratification for common disorders?

There are several discrete honours projects available in each of these research topics. If you are interested, please contact Dr William Reay (william.reay@utas.edu.au) to discuss further.

Key techniques: Genetic association studies, functional genomics, statistical genetics, genetic risk scoring, epidemiology, drug repurposing, drug discovery, normative modelling, analysis of clinical trials, computational biology, metabolomics, transcriptomics, proteomics, epigenomics

Papers of interest:

  1. Reay, W.R., Cairns, M.J. Advancing the use of genome-wide association studies for drug repurposing. Nature Reviews Genetics. 22, 658–671 (2021)
  2. Reay, W.R., et al. Genetic influences on circulating retinol and its relationship to human health. Nature Communications. 15(1):1490 (2024)
  3. Reay, W.R., et al. Genetics-informed precision treatment formulation in schizophrenia and bipolar disorder. The American Journal of Human Genetics. 1;109(9):1620-1637 (2022)

Research team: A/Prof Andrew Flies, Dr Ruth Pye, Dr Chrissie Ong, Dr Anuk Kruawan, Dr Bill Connelly

Academic Unit: Menzies Institute for Medical Research, Medical Sciences Precinct, Hobart. Students will be encouraged, but not required, to participate in field trips to work with Tasmanian devils.

Keywords: immunology, vaccines, molecular biology, cancer, immunotherapy, wildlife disease, virus, virology, CRISPR, diagnostics

Research focus:

Our team’s primary aim is to develop a vaccine to protect Tasmanian devils from the transmissible cancers that cause devil facial tumour disease. Additionally, we are interested in developing and applying immunology and advanced molecular diagnostics to better understand and control wildlife disease. Our team will soon begin vaccine trials with captive devils. We also regularly collect samples from wild devils in the field. We use samples from captivity and the field to better understand how genetically mis-matched tumour cells evade immune defenses. This feeds into our pipeline for developing a better vaccine and immunotherapies.

Research questions/topics:

  1. Engineering a devil facial tumour vaccine
    Lead researcher: Dr Andrew Flies (andy.flies@utas.edu.au)
  2. Developing an immunocontraception vaccine for invasive species
    Lead researcher: Dr Andrew Flies (andy.flies@utas.edu.au)
  3. Development of rapid diagnostic tests for wildlife pathogens
    Lead researcher: Dr Anuk Kruawan (anuk.kruawan@utas.edu.au); A/Prof Andrew Flies (andy.flies@utas.edu.au)
  4. Development of a wildlife health intelligence system (i.e., remote animal health monitoring)
    Lead researchers: A/Prof Andrew Flies (andy.flies@utas.edu.au); Dr Bill Connelly (william.connelly@utas.edu.au)
  5. Development of recombinant proteins for detection of antigen-specific immune cells
    Lead researcher: Dr Andrew Flies (andy.flies@utas.edu.au)

There are several discrete honours projects available in each of these research topics. If you are interested, please contact the specific researcher noted to discuss relevant honours projects available.

Key techniques: Synthetic virus assembly, flow cytometry, PCR, ELISA, Western blot, immunohistochemistry, microscopy, CRISPR, machine learning, recombinant proteins, cell culture, bioinformatics

Papers of interest:

  1. Kayigwe AN, Darby JM, Lyons AB, Patchett AL, Lisowski L, Liu GS, Flies AS. 2022. A human adenovirus encoding IFN-γ can transduce Tasmanian devil facial tumour cells and upregulate MHC-I. Journal of General Virology. DOI: 10.1101/2022.05.29.493930
  2. Ong CEB, Cheng Y, Siddle H, Lyons, AB, Woods GM, Flies AS. 2022. Regulation of MHC-I and MHC-II by CIITA in transmissible cancers. Open Biology. DOI: 10.1098/rsob.220208
  3. Flies AS, Darby JM, Lennard PR, Murphy PM, Ong CEB, Pinfold TL, De Luca, A, Lyons AB, Woods GM, Patchett AL. 2020. A novel system to map protein interactions reveals evolutionarily conserved immune evasion pathways on transmissible cancers. Science Advances. DOI: 10.1126/sciadv.aba5031

Applying for your Honours course

For entry into the Bachelor of Medical Research with Honours (M4G) program, you need to meet the following requirements:

  1. Students can apply for the Bachelor of Medical Research with Honours if they have successfully completed an undergraduate degree in the Bachelor of Biomedicine, Bachelor of Science, Bachelor of Paramedicine , Bachelor of Pharmacy, Bachelor of Nutrition Science, Bachelor of Exercise and Sport Science or an equivalent degree at the University.
  2. Completed the 'Steps for applying' below.

Meeting minimum entrance requirements does not guarantee entry to the Honours program as all offers are subject to supervisor and project availability.

  1. Identify a suitable project,
  2. Complete the Honours Project Application Confirmation Form (PDF 157.6 KB) in consultation with your proposed supervisor:
    1. Form available on the course page at Bachelor of Medical Research with Honours | Entry requirements
    2. Once the student section of the form is complete, please email it to your proposed supervisor, who can organise formal sign-off on the Honours project by the relevant academic unit and the Honours Course Coordinator.
  3. Complete your formal online course application form for entry into your Honours course.

There are multiple scholarships available to students undertaking research Honours in Health. Further information on the availability, eligibility, closing dates and how to apply is provided at Domestic scholarships. Students enrolling in this Honours program should apply for Health Honours Scholarships – this is an umbrella option and students will be considered for any relevant scholarships depending on their academic unit alignment and specific area of research.

Many of the scholarships are made possible by generous donations from Tasmanian businesses and individuals. Scholarship recipients may be encouraged to engage with the donors throughout the period of support.

  • For students who commence in semester 1, Honours extends from February to late October.
  • For students who commence in semester 2, the course begins in July and runs through to end of March the following year.
  • Attendance requirements will be dictated by the nature of the research project being undertaken.
  • There is an expectation that the time required to successfully complete the Honours year is ~37.5 hours per week, equivalent to a standard full-time working week.

Honours Course Coordinator

    The Bachelor of Medical Research with Honours course has projects available across the following academic units at the University of Tasmania: