Monash ‘Neuroscience in a Flash’ Competition 2020
What is the Monash ‘Neuroscience in a Flash’ Competition?
The ‘Neuroscience in a Flash’ Competition is a challenge for you, our graduate research students, to creatively present your research thesis to a general audience, in three minutes, using only one slide!
This is a great opportunity for you to take up as it will provide a platform to raise your research profile, learn valuable skills whilst also having some fun.
As a result of the current COVID-19 restrictions, we’ll be hosting the competition virtually using Zoom on:
- Session 1 (Mon 30 Nov, 12:30 - 2:00pm) - For Honours and PhD or Masters who are pre-confirmation
- Session 2 (Mon 14 Dec, 12:30 - 2:00pm) - For PhD or Masters post-confirmation
Join the fun
Share your feedback and tell us who you think should win the People’s Choice Award for the best presentation using #MonashNeuroscience on social media.
Dr Tash Thaybaranathan
Dr Anthony Filippis
Dr Karen Gregory
Dr James Coxon
Prof Terry O’Brien
Dr Karen McConalogue
30th of November
1st Place Winner: Angela (Yuxin) Fan
Presentation Title: Dissecting the Neural Substrates of Blindsight
People's Choice Award: Ting Ting Teo
Presentation Title: Astrocyte, more than just a supportive cell in CNS.
Department: Brain Research Institute (Malaysia)
Title of presentation: Using DNA methylation patterns to predict disease severity in multiple sclerosis
Department: CCS, Alfred
Abstract: Multiple sclerosis (MS) is a chronic autoimmune and neurodegenerative disease. Currently, disease management is a challenge for clinicians as they cannot predict an individual’s likely outcome at diagnosis. Published genetic biomarkers of disease severity explain up to 33% of variation in severity, suggesting that it is heavily influenced by environmental factors. Epigenetics is the biological interface of the interaction between genetic and environmental factors. DNA methylation is a dynamic and reversible epigenetic mechanism that regulates gene transcription, and is heavily influenced by environmental factors. Therefore, we hypothesised that DNA methylation plays a role in regulating disease severity in MS. In a cohort of Australian females with relapse-onset MS (n=235), we tested the association between DNA methylation patterns in whole-blood, and immune cell subsets, with disease severity. Association testing was conducted with the Chip Analysis Methylation Pipeline (ChAMP) and a false-discovery rate (FDR) of 0.05 was used to assess statistical significance. We further investigated the ability of DNA methylation to predict disease severity. We identified 745 differentially methylated positions (DMPs), enriched in the PDGFR-beta signalling pathway, and 15 differentially methylated regions (DMRs) in whole-blood. One DMR, CXCR4, has previously been associated with MS pathology. We identified 95 cell-specific DMPs in eosinophils. Using machine learning, we showed that methylation can be used to predict disease severity with an AUC of 0.91. Our results demonstrate that DNA methylation patterns are associated with, and can be used to predict, disease severity in Australian females with relapse-onset MS. Using DNA methylation patterns to predict disease severity in multiple sclerosis.
Title of presentation: Predictors of multiple sclerosis relapse activity when switching to ocrelizumab
Department: CCS, Alfred
Abstract: Over twelve disease-modifying therapies (DMTs) are approved for relapsing-remitting multiple sclerosis (RRMS) to prevent neurological relapses, a significant source of disability. Switching between DMTs is common; however evidence to support prescribing practice when switching, such as the use of a washout period, is lacking. This research aimed to identify factors associated with relapse when switching
to ocrelizumab from other DMTs (interferon-beta or glatiramer acetate, teriflunomide, dimethyl fumarate, fingolimod, or natalizumab).
Methods: Patients with RRMS who switched to ocrelizumab from another DMT were obtained from the MSBase Registry, and stratified by (1) initial DMT (DMT - the therapy before ocrelizumab), and (2) washout duration. Relapse-free survival was compared between groups. Multivariate Cox Proportional Hazards regression was used to identify predictors of time to relapse in the first year of ocrelizumab
treatment. Results: We identified 1096 patients who switched to ocrelizumab. Mean washout was 44.3 days (range 0-177 days), and 47 (4.3%) patients relapsed within one year. In univariate analysis, relapse risk was highest when switching from fingolimod (HR 2.27, 95% CI 1.27-4.07, p=0.006), and when washout duration exceeded 1 month (HR 1.96, 95% CI 1.05-3.66, p=0.035). In multivariate analysis, switching from
fingolimod remained a significant association, but only in the first three months (HR 4.00, 95% CI 1.57-10.18, p=0.0036).
Conclusion: Patients ceasing fingolimod to start ocrelizumab are at higher risk of relapse after switching. A trend to reduced relapse risk with shorter washout periods seen in this study suggests this may be one strategy to improve outcomes in such patients.
Title of presentation: Dissecting the Neural Substrates of Blindsight
Abstract: 'Blindsight’ refers to a phenomenon in which blind patients are able to respond to visual cues without conscience. When the area
of the brain that processes vision, the Primary Visual Cortex, gets damaged, a patient generally cannot see. Blindness arising from brain damage and not eye damage is referred to as cortical blindness. However, other areas of the brain are capable of rewiring and forming new connections around the damage, in an attempt to retain visual function. The alternate visual processing pathway gives way to a different type of vision, where the patient is able to respond to certain visual cues, but not consciously perceive them. They are able to avoid obstacles through simple intuition, but not identify what the obstacles are. The middle temporal area (Area MT) is a specific region in the brain that is responsible for motion sensitivity and spatial awareness and has previously been proven to be active amongst blindsight. My project will be using neural tracers injected into area MT to investigate brain areas which are active in blindsight circuitry. The infant marmoset is used as a model, as a developing brain has more regenerative potency to establish this new circuit. Connections in the brain have the potential to get stronger as they are used. Understanding the function of secondary circuits can help with the design of rehabilitative strategies to strengthen the connections, eventually leading to the improvement of clinical outcomes of those who suffer from cortical blindness.
Title of presentation: Targeting Inflammatory Mediators for the Prevention of Brain Injury in Preterm
Newborns Deparment: Hudson
Abstract: Preterm birth is currently the leading cause of neonatal morbidity and mortality worldwide,
affecting as many as 15 million babies every year. One of the leading causes of preterm delivery is the
infection and inflammation of the fetal membranes, which has adverse effects on the developing fetus.
One of the major consequences of inflammation seen in the clinical setting is neurological injury, and the
onset of neurological disorders such as cerebral palsy. The only treatment currently approved for
neurological injury is therapeutic hypothermia or infant cooling, which has shown limited clinical efficacy.
The aim of these studies is to determine which inflammatory mediators are upregulated in newborns
born less than 30 weeks of gestation, and to determine how this upregulation correlates with brain
development at time of birth, and with motor and cognitive function two years after birth. Additionally, we
aim to inhibit inflammatory mediator IL-1β and IL-6 in a preclinical sheep model of fetal inflammation, to
determine if neurological injury can be reduced. The inhibition of IL-1β by an IL-1 receptor antagonist
improved EEG power and oligodendrocyte survival, as well as reducing microglial activation and IL-1β
upregulation in the major white matter tracts of preterm fetal sheep. This was seen in conjunction with
reduced protein expression of circulating IL-1, IL-6 and IL-8. These data suggest that the inhibition of
inflammatory cytokines may be a possible treatment for white matter injury obtained during preterm
deliveries; and suggests that targeting other potent inflammatory cytokines should be suggested for
possible therapeutic interventions.
Title of presentation: Using plants to manipulate brain activity
Abstract: Information is relayed in the brain by billions of cells called neurons, which are intricately
connected to each other in a complex web. How do we know what information is being carried by which
neurons? Enter chemogenetics - a suite of tools that allow us to only activate the neurons we want using
specific drugs. It represents a useful weapon in a neuroscientist’s arsenal as it allows for elucidating the
relationships between brain activity and physiological function. When chemogenetic receptors are
activated, it hijacks normal neuronal communication by manipulating which neurons fire and which
neurons do not. This is invaluable given the vast connections that exist between neurons, and thus,
dictating which neurons are activated whilst silencing the background noise from the others allows us to
probe its activity and functions. Chemogenetics thus helps us delineate this complex brain circuitry and
identify the key players involved in modulating specific functions and behaviours such as hunger, sleep,
addiction and breathing. My research explores whether it is possible to control, manipulate and delineate
brain activity using plants.
Title of presentation: Diet, lifestyle and disease outcomes in multiple sclerosis patients.
Department: CCS, Alfred
Abstract: Despite inconclusive evidence regarding dietary interventions for multiple sclerosis (MS) people with MS report interest in diet to manage disease outcomes. This pilot study aims to understand dietary habits among MS patients and to investigate whether certain dietary patterns, sleep, or exercise influence disease outcomes. Participants, recruited from the Alfred Hospital completed a case report form capturing demographics, physical activity, diet use and sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI). Participants also completed the Australian Eating Survey, which captures average nutrient/food intake over the last 6 months. Clinical information regarding disease activity, treatments and disease durations were obtained from the MSBase registry. Univariable poisson regression analysis was used to look at associations between lifestyle factors and relapse. Univariable linear regression was used to examine associations between lifestyle factors and disability. Of 53 participants, 38% reported using a special diet for MS. Among diet users, the Mediterranean diet (15.2%) was the most popular. High fat and high sugar consumption did not predict disability or relapses. Similarly, diet quality did not predict disability and relapses either. However, multivariable linear regression demonstrated that every one-point increase on the PSQI was associated with a 0.19 increase in the disability scores (p<0.05). Likewise, one-hour increase in exercise per week was associated with a 0.24 decrease in disability scores (p<0.01). These findings suggest that high fat and sugar consumption or diet quality alone do not influence disease outcomes. Lifestyle factors, including sleep and exercise and different dietary components, may play a role.
Title of presentation: Age-related changes in astrocyte reactivity and function in the marmoset brain
Abstract: Why do we start to lose memory and cognitive abilities with ageing? Our memory and cognitive abilities depend on the connection between neurons called synapses. However, with ageing, synapses excessively eliminated in brain areas important for memory and cognition such as frontal parts of our brain. This is thought to be the main cause of the decline in memory and cognitive functions with ageing. Many postulate that excessive loss of synapses in the ageing brain is due to the changes in cells that govern synapses. Astrocytes are part of the glial cell populations which are distinct from neurons. They help to form, mature and eliminate synapses in our brain. However, with ageing, astrocytes start to become reactive and lose their normal functions. Are the alterations in astrocyte function really driving the loss of synapses in brain regions responsible for cognition and memory? Our project explores the changes in astrocyte reactivity and function in the frontal brain important for cognition and memory. We use the marmoset brain that can closely represent highly complex human frontal brain regions. Astrocyte reactivity was upregulated in brain regions important for cognition and memory such as dorsolateral prefrontal cortex (dlPFC), anterior cingulate cortex (ACC), and hippocampus CA1 of the marmoset brain. In addition, we show that reactive astrocytes in the ageing brain had increased capacity to eliminate synapses in brain regions important for cognition and memory.
Title of presentation: Astrocyte, more than just a supportive cell in CNS.
Department: Brain Research Institute
Abstract: Astrocytes comprise nearly half of the brain's cells and have been regarded as the supportive cells in the CNS. They support the neuronal functions by regulating the synaptic homeostasis, providing structural and metabolic support to neurons, and maintaining the blood-brain barrier. However, studies over the past 20 years show that astrocytes play an important role in synaptic formation. Due to the close proximity and functional integration between the astrocytes peripheral processes and neurons, the term ‘tripartite synapse’ was coined to explain the structure. The intimate association of the components of tripartite synapse suggests that the formation of synapses is no more an intrinsic property of those neurons but can be profoundly regulated by extrinsic signals. Astrocytes have been found to increase the synapse number and stability. Moreover, astrocytic secretion factors are involved in forming, stabilizing, and eliminating synapse through various downstream mechanisms of the synaptic cell adhesion molecules. Accumulating evidence shows astrocytes are also implicated in the pathophysiology of depression. The underlying pathophysiology of depression is still not clearly known, and the limiting factors of the current treatments are driving searches for better therapeutic targets. Hence, we will determine which the astrocytic secretion factors, under the stress condition, affect the formation of synapses of serotonin neurons, particularly. Besides, we would like to know if altered synaptic formation will affect serotonin level production, which has been considered one of the main chemicals underlying the pathophysiology of depression.
Title of presentation: The little brain of the gut in Hirschsprung disease
Abstract: The gut is the only peripheral organ with its own nervous system called the enteric system (ENS) or 'the little brain of the gut'. This little brain regulates nearly all gut function including digestion, nutrient absorption, waste excretion and gut motility. Hirschsprung disease (HSCR) is a congenital disorder caused by ENS dysfunction, whereby the distal bowel lacks nerves. Newborns with HSCR present symptoms including chronic constipation, growth insufficiency, bowel obstruction, inflammation and if untreated, death. The mainstay of treatment for HSCR is surgery, where the diseased section of the intestine is removed or bypassed. Surgery is life-saving but not curative and patients may experience postsurgical complications which raises the question- are the normal segments actually normal? To facilitate enhanced diagnosis, treatment and prevention, a better understanding of the pathophysiology is required. As part of my PhD project, I will be investigating gut segments from HSCR surgeries, using advanced microscopy techniques. This will help us compare HSCR-affected gut tissue with healthy gut and achieve a greater understanding of this disease on a cellular and molecular level. Majority of current evidence is based on animals, which does not always translate well to humans, thus our study should provide invaluable data on HSCR pathophysiology that is clinically relevant. We hope that by better understanding these microscopic changes to the ENS in patients with HSCR, we will unravel how these changes influence disease phenotypes and potentially find new treatment targets so that one day, surgery is not the only option.
14th of December
Title of presentation: Human Motherhood is Neuroprotective for the Late-Life Maternal Brain
Abstract: The maternal brain undergoes structural and functional plasticity during the transition to motherhood. Although we have a growing understanding of the brain changes associated with pregnancy and the early postpartum period, very little is known about their time-course - whether they endure throughout the lifespan - and what these changes mean for the ageing trajectory. We are first to investigate the relationship between parity (i.e. number of children) and cortical thickness, resting state functional connectivity, and memory performance in a large sample of late-life women (N=226). We show a positive correlation between the thickness of the parahippocampal gyrus (a region associated with memory) and the number of children parented. This is consistent with our cognitive results, showing a positive correlation between verbal memory performance and number of children parented. We also show decreased resting state functional connectivity between, but not within, networks and hemispheres, and decreased connectivity from the prefrontal cortex. All three of these patterns are shown in the opposite direction in studies of age-related decline, suggesting motherhood confers a neuroprotective effect on brain function in late-life. Our results show a consistent pattern across brain structure, function and cognition that is indicative of a neuroprotective impact of motherhood on the ageing maternal brain. This research is the first to explore the ageing parental brain in humans, and provides the first insight into the long-lasting, and potentially beneficial neural adaptations to parenthood for the structure and function of the maternal brain in late-life.
Title of presentation: Silencing hyper-activated immune cells in the brain with a scorpion toxin analogue
Abstract: Alzheimer's now affects 50 million people worldwide. Part of the fear around Alzheimer's stems from the sense that there's nothing we can do about it. Despite decades of research and billions of dollars spent in clinical trials, we still have no disease-modifying treatment and have a problem with drug delivery to the brain. There are many steps involved in the molecular cascade that causes the clinical symptoms of Alzheimer’s disease, and identifying which step to try to block is complex. Recently, a critical step in the process was identified, which is hyper-activation of the immune cells (microglia) in our brain. My research efforts include delivery of a novel peptide toxin (HsTX1) derived from a scorpion to the brain in order to specifically block this step and stop the disease. However, it remains a challenge to get the peptide into the brain. Shuttle peptides are versatile vehicles that travel to the brain, so why not add an extra passenger? To do this, we decided to deliver HsTX1, and we’ve added two special molecules. One is a linker, which acts as a glue that binds the HsTX1 to the shuttle peptide, and the second is a brain-targeting shuttle peptide. When you put both of these together, you have a drug delivery system to the brain. To test this, we will employ live imaging techniques to track its pathway to the brain.
Title of presentation: Investigations of multiple sclerosis and modifiable influences: the effects of vitamin D
status and pregnancy
Department: CCS, Alfred
Abstract: Multiple sclerosis (MS) is one of the most common disabling neurological conditions among young adults. The latitudinal incidence gradient is one of the strongest risk factors for MS. It is hypothesised that UV exposure and vitamin D status are involved in explaining this observation. Epidemiological studies have also suggested a significant association between vitamin D deficiency and MS risk. It is well established that vitamin D has immunomodulatory effects on innate and adaptive immune cells. Vitamin D receptor-binding is enriched in regions of MS risk variants. Few studies have explored the effects of vitamin D on immune cell function in the in vivo context. Pregnancy is also known to have immunomodulatory changes. Historical observations showed reduced relapse activity during pregnancy, but it is unclear whether this remains true in the modern era with availability of MS treatments.
We aim to examine the effects of vitamin D on immune cell subsets in healthy controls and MS cases, in regards to gene expression and circulating immune cell phenotype. We will also explore whether there are differences in response between people with and without MS. The predictors of relapse in pregnancy in the modern era of effective therapies will be examined using MSBase, the largest international registry of MS patients. This project will provide significant insights into how two important factors interact with MS risk and disease activity, and will further our clinical as well as pathophysiologic understanding of MS.
Title of presentation: Development of personalized ‘disease-in-a-dish’ model of focal cortical dysplasia using induced pluripotent stem cells
Department: CCS, Alfred
Abstract: Focal cortical dysplasia (FCD) is a type of malformation of cerebral cortex and abnormal cytoarchitecture linked to disruption in the mTOR pathway, and is among the most common pathologies causing drug-resistant epilepsy. A range of somatic and germline mutations in mTOR pathway genes have been associated with FCD. Conventional animal-based models are unable to recapitulate the complex pathophysiological mechanisms of FCD. Here, we developed a ‘personalised’ human-based model using induced pluripotent stem cells (iPSCs) obtained from individual patients with FCD. Methods: A patients with loss-of-function mutation in the mTOR pathway gene, DEPDC5, was identified through whole genome sequencing. Peripheral blood mononuclear cells were prepared from the patients to generate iPSCs. Using these iPSCs, monolayer neurons and 3D brain organoids were generated. Their morphology, neuronal gene expression and electrical activity was studied using immunocytochemistry and microelectrode array (MEA) analysis.
Results: Monolayer neurons derived from patients’ iPSCs expressed pre-plate (TBR1), deep layer (CTIP2) and surface layer (Satb2) cortical neuronal markers, including general neuronal markers (Map2,Tau, Î²-III) and calcium binding protein (Calbindin). Action potential based neuronal activity measured by MEA showed higher spike frequency in monolayer neurons derived from patients compared to control neurons. 3D brain organoids have been generated; characterization is underway and will be presented. Discussion: We have developed ‘disease-in-a-dish’ models from patients with FCD. These models may provide novel insight into pathophysiological mechanisms that underpin FCD-related drug-resistant epilepsy involving mTOR pathway, and could be used as ‘personalised’ drug screening platform in individual patients with FCD.
Title of presentation: Probing the Metabotropic Glutamate Receptor 5 (mGlu5) Activation Network: Discovery of Residues that Govern Receptor Activation
Abstract: The metabotropic glutamate receptor 5 (mGlu5) is a class C G protein-coupled receptor (GPCR) that has emerged as a promising drug target for multiple central nervous system disorders. Structurally, mGlu5 forms obligate dimers. Each protomer possesses a 7-transmembrane (7TM) domain which is connected through a cysteine-rich domain (CRD) to a large extracellular domain (ECD), encompassing the orthosteric ligand-binding Venus flytrap domain (VFD). Recent spectroscopic studies on mGlu5 signaling demonstrated large-scale conformational changes underlie signal transmission from the ECD to the G protein coupling 7TM domain. Although these studies reported the necessity of extracellular loops (ECL) for activation of mGlu5 by orthosteric agonists, specific residues related to activation remain unknown. In the current study, a combination of sitedirected mutagenesis and functional Ca2+ mobilisation studies identified residues within the mGlu5 ECLs that aid in the propagation of orthosteric agonist-induced conformational changes in the VFD to the 7TM. Mutation of ECL2 residues P715, D717, M719, P723, S724 and R726 markedly reduce the action of glutamate and thus may contribute to the mGlu ¬5 activation network. Interestingly, mutation of Y729 leads to compromised signaling of the glutamate which can be rescued by using positive allosteric modulator (PAM). Y729 may therefore play an important role in the functional coupling of VFD with the 7TM domain. Overall, the reduction of maximal signalling response with glutamate of the ECL2 mutants suggests that these residues serve as a rigid fulcrum to relay the agonist binding at the VFD to the intracellular G protein coupling region of the 7TM domain.
Title of presentation: The cost-effectiveness of chronic disease management plans in stroke
Abstract: Stroke imposes a substantial economic burden in Australia. The Government of Australia has introduced Chronic Disease Management (CDM) plans which aim to provide better management of risk factors in people with stroke. General practitioners (GP) are financially encouraged to use CDM plans. Despite the efforts and commitments of the health care stakeholders, there is limited evidence of cost-effectiveness of these CDM plans. The overall aim of my project is to evaluate the cost-effectiveness of CDM plans compared to usual GP care in stroke. This study will incorporate a retrospective cohort study of patients with stroke from two Australian states using data linkage. Costs of healthcare resources utilised after stroke will be compared to prior to stroke to estimate costs attributable to stroke, and then compared between those who were or were not provided a CDM plan. The study will enable us to provide recommendations to policy makers about CDM plans in stroke that should be utilized or modified in clinical practice. It will also provide information on the feasibility of performing an economic evaluation based on data linkage at a cross-jurisdictional level.
Title of presentation: Hitting close to home: concussion in Australian collision sport
Department: CCS, Alfred
Abstract: The issue of concussion in sport has been thrown into the spotlight in recent years. The blockbuster movie ‘Concussion’ starring Will Smith, has shed light to the concussion catastrophe in NFL football. However, this realisation has taken longer in Australia. Collision sports are an integral part of Australian culture, with events such as the AFL grand final and state of origin two major sporting and now cultural events of the year across many states. Not to mention the millions of children and adults that partake in Australian football and rugby leagues worldwide. However there has been some scepticism to the effects of concussion in these sports with some suggesting ‘were different to American collision sports’. However, we’re finally seeing this issue hit close to home, with the first ever cases of chronic traumatic encephalophagy (CTE) discovered in Australian collision sport athletes in the last year; in two ex-Rugby league players and more recently ex-AFL player Polly Farmer. CTE is irreversible brain damage linked to repeated concussion that can only be diagnosed at death, but can cause personality changes, cognitive decline, mental health problems. We currently lack research into the effects of concussion in Australian collision sports. Primarily we aim to develop more objective and sensitive tools to better diagnose concussion, monitor recovery, and return-to-play decisions and minimise immediate and future brain damages.
Title of presentation: Bridging the research valley of death: neural stem cells for cerebral palsy
Abstract: Brain injury around the time of birth can lead to significant neurological and cognitive deficits, as well as cerebral palsy. Neural stem cells (NSCs) may be able to alleviate this injury and have been shown to engraft and even replace dead and dying cells in the injured brain. As part of my PhD, I am conducting pre-clinical neonatal rat studies that aim to optimise NSC therapy for effective translation into humans.
Translation is often halted by the phenomenon know as the ‘valley of death’; a gap from pre-clinical research to implementation and uptake in humans. One solution is better informed pre-clinical research that increases acceptability with consumers, in this case, the cerebral palsy community. In conjunction with my pre-clinical work, I am conducting an online survey that asks the cerebral palsy community, Is NSC therapy acceptable? Are there ethical concerns with NSCs? What level of risk is deemed acceptable for potential benefit? Survey responses can contribute to informing our future research and ensuring acceptability of NSCs. By undertaking this survey coupled with necessary pre-clinical research, I hope I can bridge the ‘valley of death’ and help to mark a path towards developing a clinically relevant NSC therapy.
Title of presentation: The role of the neurokinin-1 receptor in ischaemic stroke-related neuroinflammation
Abstract: Ischaemic stroke affects millions of people worldwide every year, and two fifths of patients either die or suffer from permanent disability. Current therapies have a narrow window of administration and a multitude of exclusion criteria, and thus many patients are not able to receive treatment. Additionally, if blood flow is able to be restored, a subsequent neuroinflammatory event known as ‘reperfusion injury’ can occur, which can lead to further tissue damage and hinder functional recovery. It is critical to investigate therapeutic targets that could be used as adjunct therapies, in order to minimise inflammation post-stroke and improve clinical outcomes. One such target is the neurokinin-1 receptor (NK1R), which is well-known to contribute to inflammation and edema in peripheral vasculature and is currently being clinically investigated for brain trauma. Current in vivo studies have also indicated that NK1R antagonists may be promising for minimising cerebral edema and neuroinflammation associated with ischaemic stroke. However, the mechanism of action and precise processes through which NK1R contributes to stroke pathophysiology remains unclear. This project will investigate neuro-immune interactions and characterise cellular mechanisms at the blood-brain barrier to understand how the NK1R contributes to ischaemic stroke-induced neuroinflammation. Further studies with selective antagonists will also determine the usefulness of inhibiting the NK1R to minimise the inflammatory response, as an adjunct therapy to thrombolytic agents during the acute treatment phase.
Prior to the event
Prior to the event, the host will be required to meet with the event organisers to run through what’s expected from them, understand who else will be participating in the event and discuss the overall agenda. One week prior to the event, the host will attend a practice session conducted via Zoom.
During the event
Member of the Monash Neuroscience Executive Committee, Professor James Bourne (Chair) to open the event and introduce the host.
The host will be responsible for:
- Introducing each finalist as per the provided run sheet and explaining competition rules and judging criteria
- Timing each speed thesis presentation to ensure it does not exceed three minutes and ring the timer bell when presentations exceed the time allocated
- Directing judges to the breakout room
- Announcing winners
- Presenting our successful recipients with virtual certificates
Prior to the event
- In the case that there are more than 6-8 student applications, judges will be responsible for assessing applications and selecting finalists to compete in the competition
- Judges must be well versed in competition rules and judging criteria
- One week prior to the event, all judges will be required to attend a briefing session.
During the event
Judges will be responsible for:
- Attending the virtual event and watching each three minutes thesis presentation
- Assessing each presentation against judging criteria provided (assessment sheet will be supplied prior to the event)
- Ensuring each presentation adheres to competition rules
- Tallying up assessment sheets and determining winners
Judges must ensure the recipient of each award has:
- Presented their thesis in an understanding way, explaining the background and significance to the research question being addressed. Whilst also explaining terminology clearly.
- Conveyed enthusiasm for their research, maintained their audience's attention and carefully presented to not trivialise or generalise their research.
Judges will follow the below criteria and allocate an overall score to select a recipient for each prize. The broad principles the judges will be guided by are:
Monash ‘Neuroscience in a Flash’ Competition Prizes
- 1st place winner: $300
- People’s Choice Award $200