Neuroimmunology Australia

Webinars

A new initiative for Neuroimmunology Australia in 2020 was the introduction of a webinar series.

Each one hour webinar consists of two presentations, which commence at 12 noon (QLD) / 1 pm NSW/VIC/TAS summertime / 10 am (WA) / 02:00 (UTC).

To receive notifications and zoom links to upcoming webinars, or if you would like to participate as a speaker, please contact our coordinator, A/Prof Markus Hofer. Alternatively, click on the red coloured date below to join the meeting.

Webinar Schedule 2023

Friday 30th June 2023

Speaker 1:
Dr Ebony Monson, La Trobe University
Title: The antiviral role of lipid droplets in the brain
Summary: The role that lipid droplets (LDs) play in the antiviral response in the brain is starting to be uncovered. We recently discovery that LDs are rapidly upregulated in response to early infection of multiple viruses that infect the brain (ZIKV, DENV and HSV-1). In particular, astrocyte cells are the main contributor to the upregulation of LDs in the brain and this upregulation drives the production of effective type I /III interferon responses to combat infection. To better understand the mechanism behind this antiviral role of LDs, we have described the distinct proteome changes on virally driven LDs, which changes to include important antiviral proteins. Our work positions the LD as an important signalling platform during this the early innate antiviral response. 

Speaker 2:
Sasha Maximova, University of Sydney
Title: Exploring cell senescence in neurodegeneration
Summary: ALS is a neurodegenerative disease involving upper and lower motor neuron death. Survival prognosis is 3-5 years following diagnosis, and there is no effective treatment available. Senescence has been recently identified as a potential avenue for exploring new drug targets in treating ALS, due to the role senescence plays in chronic inflammation and associated neuronal cell death. This project focuses on characterising iPSC-derived astrocytes and microglia and their involvement in senescence and its associated secretory phenotype, to help identify potential drug targets and better understand underlying molecular signalling pathways.

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Friday 26th May 2023

Speaker 1:
A/Prof Alessandro Castorina, School of Life Sciences, UTS
Title: VPAC1 and VPAC2 heterozygosity reveals divergent biological activities of the receptors in BV2 microglia – relevance to multiple sclerosis pathogenesis
Summary: Multiple sclerosis (MS) is a multifactorial immune-mediated disease of the central nervous system (CNS). Key pathogenic mechanisms involve the infiltration of peripheral lymphocytes and consequent polarisation of microglial cells. The vasoactive intestinal peptide (VIP) is a neuropeptide broadly involved in the modulation of inflammatory responses and its activity is mediated by two G protein-coupled receptors, VPAC1 and VPAC2. Previous reports from VPAC1-null mice subjected to experimental autoimmune encephalomyelitis indicate ameliorated pathology in these mice, whereas VPAC2-null mice show disease exacerbation. Based on these findings, we used CRISPR-Cas9 gene editing to develop two stable heterozygous BV2 microglial cells (VPAC1+/- and VPAC2+/-), which were used to evaluate the biological and molecular features of microglia at baseline and during an inflammatory challenge. Our results indicate that partial VPAC1 or VPAC2 gene ablation conferred distinct biological characteristics to BV2 microglia, pinpointing the importance of these neuropeptide receptors in the fine-tuning of microglia responses in CNS diseases characterised by an inflammatory component, such as MS.

Speaker 2:
Dr Ellen Gillespie, University of Queensland
Title: Understanding the role of neutrophils in the acute phase of spinal cord injury 
Summary: Neutrophils are thought to play a large role in secondary inflammatory pathology during the acute phase of spinal cord injury (SCI). Historically, neutrophils have been seen as one broad cell type that are a major perpetrator of secondary damage to the injured spinal cord. However, recent findings have begun to recognise distinct neutrophil subsets that each have unique functions dependent on their maturation state and gene expression profile. We have used single-cell RNA sequencing and transgenic mouse models to track how SCI affects neutrophil production, recruitment and function, paving the way for further studies to delineate specific roles for neutrophil subsets following SCI.

Friday 31st March 2023

Speaker 1:
Dr Caitlin Finney, Westmead Institute for Medical Research, Sydney
Title: Using machine learning to uncover novel gene candidates in Alzheimer’s disease 
Summary: Most of what we know about Alzheimer’s disease (AD) has come from models of familial AD, which accounts for a small minority of cases. Very little, however, is known about late onset AD (LOAD), the most common form accounting for >95% of cases. With this in mind, we sought to take a new approach to understanding genes that may be involved in LOAD and asked can machine learning tell us anything about biology? It turns out that it probably can. We use machine learning to analyse the brain gene expression data of LOAD patients and, in doing so, uncover novel gene candidates and highlight a role for mitochondria in LOAD pathogenesis.

Speaker 2:
Haidyn Bulen, University of Sydney
Title: Exploring the role of the complement system in IL-6- and IFN-a-induced neuroinflammation
Summary: Chronic interleukin-6 or interferon-alpha production in the central nervous system lead to diseases such as neuromyelitis optica spectrum disorder and Aicardi Goutières Syndrome. Understanding the molecular mechanisms of cytokine-driven disease is vital for the development of novel and potentially disease-modifying treatments. To address this, we probed transcriptomic data from transgenic mice that overexpress either interleukin-6 or interferon-alpha in the brain and found a robust upregulation of the complement system. We next administered a complement inhibitor that antagonized the receptor for the potent anaphylatoxin C5a to each respective mouse line. Our results indicate that blocking complement C5aR1 has a limited impact on resolving the disease driven by interleukin-6 or interferon-alpha overproduction and is thus a non-optimal target for the treatment of diseases in which these cytokines play a pathological role. 

Recordings of previous webinars

Thanks to all of our presenters who have agreed to make their presentations available online.

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