UQ Neuro

20/03/2026

🎓QBI Neuroseminar🎓
Note: not available with zoom

Prensented by A/Professor Rachel Hill
Behaviour Neuroscience Laboratory
Department of Psychiatry
Monash Medical Centre

Time: 12 - 1PM
Date: 25th March
Location: QBI L7 Auditorium
Abstract:
Infections during pregnancy are well known to increase risk for the offspring to develop a neurodevelopmental disorder later in life. Of imminent concern then is the risk that COVID-19 infection may cause to the unborn fetus. To this end we established a multisite birth cohort study of infants exposed to COVID-19 in utero from Melbourne, Australia and Londrina, Brazil. Our published data shows poorer neurodevelopmental outcomes at 12 months of age in infants exposed to severe SARS-CoV-2 infection as well as altered DNA methylation of genes associated with synaptic pathways. Unpublished data from the 2-year-old time point shows altered communication and language as well as higher scores on the Autism diagnostic observation scale (ADOS) in infants exposed to SARS-CoV-2 in utero, as well as altered DNA methylation of 17 genes across both Melbourne and Londrina sites. Site replication in two distinct populations adds significant weighting to the significance of these findings. These data are now being reverse translated back into both human induced pluripotent stem cell and animal models to understand the brain mechanisms that link SARS-CoV-2 exposure to adverse brain and behaviour function. Preventative as well as restorative treatment targets are being investigated in these preclinical models to ultimately improve outcomes in infants exposed to infections in utero.

Check out our link in bio for more information!!

17/03/2026

🎓QBI Neuroseminar🎓
Note: not available with zoom

Long non-coding RNA in the regulation of complex behaviour
Presented by A/Professor Kelly Clemens
School of Psychology
University of NSW

Time: 12 - 1PM
Date: 18th March
Location: QBI L7 Auditorium
Abstract:
Long non-coding RNAs (lncRNAs) are emerging as powerful regulators of gene expression, yet their roles in complex behavioural processes remain largely unexplored. In this seminar, Associate Professor Clemens will present new insights into how lncRNAs may act as master regulators of behaviour, bridging RNA biology with neuroscience and psychology.

Check out our link in bio for more information!!

10/03/2026

🎓QBI SEMINAR🎓
Note: Not available via Zoom

Synaptic and Glial Mechanisms of GABA-A Receptor Dysfunction in Epilepsy
Presented by Dr. Nela Durisic
Queensland Brain Institute
University of Queensland

Time: 12-1pm
Date: 11th March
Location: QBI L7 Auditorium
Abstract:
The GABA-A receptor (GABAAR) is a central mediator of both phasic and tonic inhibition in the brain, and pathogenic variants in its subunits are increasingly recognised as important causes of severe paediatric epilepsies. In this seminar, I will present new data examining how distinct receptor variants differentially alter inhibitory signalling, receptor surface expression, and nanoscale organisation at neuronal synapses and in astrocytes.

By dissecting the underlying mechanisms, we distinguish reduced inhibition resulting from impaired receptor trafficking and decreased surface stability from dysfunction caused by altered channel conductance, and relate these molecular mechanisms to clinical severity. Notably, variants that enhance receptor activity can paradoxically be associated with particularly severe phenotypes, and I will present at least one explanation for this. I will also show that profound receptor dysfunction affects excitatory synapse maintenance and that, in cortical astrocytes, epilepsy-associated variants drive context-dependent changes in receptor organisation influenced by neuron–glia interactions.

Together, these findings highlight how altered localisation of GABAARs in neurons and astrocytes destabilises excitation–inhibition balance, leading to inhibitory failure in cortical networks and contributing to diverse epileptic phenotypes. Finally, I will discuss a potential therapeutic avenue leveraging these mechanistic insights that involves drug repurposing.

Check out our link in bio for more infomation!!!

03/03/2026

🚨 LOCATION ANNOUNCED 🚨

Our Welcoming Event 2026 will be held at 📍 ModWest 11A-131

Get excited to meet fellow members, make new friends, and hear about all the exciting plans we have for the year ahead 👀✨️

Dont forget to visit the link in our bio or scan the QR code!!

We can’t wait to see you there :dizzy:
🔗 https://campus.hellorubric.com/?eid=53365

02/03/2026

Join us at the UQNS Welcoming Event 2026 to meet fellow members, make new friends, and enjoy fun bonding activities 🤩

We’ll also be sharing a sneak peek of our exciting plans for the year ahead — you won’t want to miss what’s coming 👀✨️

🎉 UQNS Welcoming Event 2026
🗓 13 March 2026
⏰️ 6:00PM – 8:30PM
🍕Food: Pizza and Soft Drinks
📍Location: TBA (UQ St Lucia Campus)
🎟 FREE — Exclusive to UQNS members only

Secure your place via the link in our bio or scan the QR code 🔗 https://campus.hellorubric.com/?eid=53365

02/03/2026

🎓QBI Neuroseminars🎓
Note: not available via Zoom

The twilight of the aggresome: from self-exile to the rise of new defensive compartments
Presented by Dr. Zhaoyu Li
Queensland Brain Institute
University of Queensland

Time: 12-1pm
Date: 4th March
Location: QBI L7 Auditorium
Abstract:
Neurons are constantly challenged by proteotoxic stress during aging, a key driver of neurodegenerative diseases. Aggresomes are well-recognized quality-control compartments that sequester misfolded proteins and facilitate their clearance. However, we found that aggresomes themselves undergo functional decline and become damaged under sustained proteotoxic conditions. As long-lived cells, how neurons adapt to the deterioration of this primary defense system remains poorly understood. Using C. elegans models expressing neurodegenerative disease–associated misfolded proteins and tracking individual neurons across the lifespan, we observed that large, damaged aggresomes are not efficiently degraded intracellularly. Instead, they are expelled from the soma through a previously uncharacterized process, in which the aggresome is extruded via a filopodium-like structure. Strikingly, dysfunction of aggresomes also triggers the emergence of another type of quality-control compartment, which we term SolAS (Soluble misfold protein-triggered Axonal Swellings). These structures sequester soluble misfolded proteins into neurites, redistributing proteotoxic burden away from the soma, and facilitate their clearance via exophers and microvesicles. Together, extrusion of damaged aggresomes and the formation of SolAS act cooperatively to remodel proteostasis capacity and maintain cellular integrity, ensuring continued protection of neurons as primary quality-control systems decline with age.

Find out more in the link in our bio!!

23/02/2026

20/02/2026

🎓QBI Postdoctoral Seminars🎓

Atlastin dysfunction linked to Tau pathology in Hereditary Spastic Paraplegia
Presented by Dr. Juan Carlos Polanco

Engineering Antibody Therapeutics for Tauopathies
Presented by Dr. Esteban Cruz Gonzalez

Time: 12-1pm
Date: 25th Feb
Location: QBI L7 Auditorium
Abstract: Link in our bio

Find out more in the link in our bio!!