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Monash ‘Neuroscience in a Flash’ Competition 2020

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.

Judges

Dr Tash Thaybaranathan

Dr Anthony Filippis

Dr Karen Gregory

Dr James Coxon

Prof Terry O’Brien

Dr Karen McConalogue

Finalists

30th of November

1st Place Winner: Angela (Yuxin) Fan
Presentation Title: Dissecting the Neural Substrates of Blindsight
Department: ARMI

People's Choice Award: Ting Ting Teo
Presentation Title: Astrocyte, more than just a supportive cell in CNS.
Department: Brain Research Institute (Malaysia)

Pia Campagna

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.

Michael Zhong

Angela (Yuxin) Fan

Sharmony Kelly

Amira Mohany

Manisha Deekiri Kewage Dona

Dongyu Rim

Ting Ting Teo

Narges Mahdavian

14th of December

Winnie Orchard

Sanjeevini Babu Reddiar

Wei Yeh

Muhammed Javaid

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.

Monash ‘Neuroscience in a Flash’ Competition Prizes

1st place winner: $300
People’s Choice Award $200

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