Abstract Submission
Plenary Speakers
Carlos Matute, PhD
Professor, Department of Human Anatomy, Faculty of Medicine, University of Zaragoza, Spain.
Ricardo Miledi Honorary Professor in Autonomous National University of Mexico
Elected Member of the Academia Europaea
Alexander von Humboldt Fellowship Recipient
Professor Matute is a neurobiologist specializing in oligodendrocytes, myelin, and neurodegenerative diseases. His Laboratory of Neurobiology at the University of the Basque Country, studies the cell biology of neurotransmitter receptors in glia (astrocytes, oligodendrocytes, and microglia) and their functional and pathological roles. His ground-breaking work has demonstrated that excessive activation of excitatory receptors damages oligodendrocytes and triggers demyelination in multiple sclerosis and stroke. Over the past decade, he has shown that neurotransmitter receptors in microglia and oligodendrocytes can regulate energy metabolism, modulate neuroinflammation, and promote myelin repair, and uncovered molecular and cellular mechanisms in neurone and glia contributing to Alzheimer's and Parkinson's diseases—findings with strong translational relevance.
Chris Reid, PhD
Professor, Lead of the Epilepsy and Neurodevelopment Research Priority,
Head of the Neurophysiology of Excitable Networks Laboratory
The Florey Institute of Neuroscience and Mental Health
Professor Reid is Research lead of the Epilepsy and Neurodevelopment Research Area and heads the Neurophysiology of Excitable Networks Laboratory at The Florey. He is a translational neuroscientist and leads a multidisciplinary team that investigates the molecular and cellular causes of epilepsy. Key work from his lab includes developing and characterising new genetic models of epilepsy and identifying new molecular targets for treating this devastating disease. Professor Reid has strong engagement with industry and clinical partners providing a translational path and is research vision is to continue to drive pre-clinical programs that will create and validate therapeutic strategies targeted at genetic causes of epilepsy and other neurological disorders.
Mouse modelling of genetic epilepsy: a ‘tail’ of divergence and convergence
Our understanding of the genetic architecture of epilepsy has increased exponentially recently, with over 900 causative genes now implicated. Developmental and epileptic encephalopathy (DEE) are the most severe of the genetic epilepsies characterized by drug resistant seizures and a host of additional symptoms including gait, cognitive and social deficits. There is significant heterogeneity within the DEEs with treatment needed to be tailored to the specific genetic cause. Understanding this heterogeneity is therefore key to better outcomes for people with DEE. The disease is mostly a monogenic disorder that can be modelled by knocking in specific human genetic causes into mice. In this talk I highlight the benefits of modelling DEEs in mice. I will show how mechanisms in DEE mice caused by different genetic variants can diverge and converge with implications for treatment. I will also highlight how these mice could be used to devise and test precision therapeutics. Finally, I will touch on sudden unexpected death in epilepsy in DEE and how mouse modelling may help understand the cause and suggest a common treatment.
Wickcliffe (Cliff) Abraham, PhD, FRSNZ
Professor, Department of Psychology
Poutoko Taiea Distinguished Chair
University of Otago
Professor Cliff Abraham a long-standing research interest and expertise in the mechanisms of synaptic plasticity, metaplasticity and memory formation in the brain. My clinically relevant research interests include biomarkers and therapeutics for Alzheimer’s disease and other dementias, neurogenesis and neuroprotection mechanisms using animal and cell-based models.
Professor Abraham has published nearly 200 journal articles, books and book chapters and has been awarded a number of number of prestigious prizes and awards. These include a James Cook Fellowship, the Marsden Medal and the Rutherford Medal recognising exceptional, career-spanning contributions to knowledge, science, technology, or the humanities, highlighting sustained research impact, service, and leadership in New Zealand.
Professor Abraham is retiring in 2026 and it is an honour to have Cliff, who was a founding member of AWCBR, giving one of the plenary talks at AWCBR 2026.
Transregional metaplasticity in health and disease
Synaptic plasticity is fundamental to learning and memory storage. Not surprisingly, it is a highly regulated process. This includes regulation by the history of prior activity in the learning networks through processes termed metaplasticity. Metaplasticity has typically been studied in local synaptic networks. Previously, we showed that long-term potentiation (LTP) in area CA1 of the hippocampus is inhibited by prior synaptic activity in that region, via bidirectional communication with astrocytes. This process involves release of the gliotransmitter tumour necrosis factor (TNF), and accounts for impaired LTP in a mouse model of Alzheimer’s disease. We now have evidence that this metaplasticity effect unexpectedly crosses from CA1 to a completely different region of the hippocampus, the dentate gyrus. This effect is mediated by muscarinic and metabotropic glutamate receptor activation of calcium signalling in astrocytes followed by release of TNF that acts in a paracrine fashion on astrocytes, ultimately leading to the release of glutamate acting on GluN2B-containing NMDA receptors to inhibit LTP. Interestingly, this novel transregional signalling cascade is contradirectional to the normally described information flow from the dentate gyrus to CA1 via CA3. Thus, there is unexpected communication between hippocampal subregions, mediated by astrocytes, that may play an important role in information processing and storage under normal conditions, and that may contribute to impaired cognition when aberrantly engaged in neurological disease.