Anthony J Hannan — ASN Events

Anthony Hannan

Florey Institute of Neuroscience and Mental Health, University of Melbourne, VIC, Australia

Professor Hannan received his undergraduate training and PhD from the University of Sydney. He was then awarded a Nuffield Medical Fellowship at the University of Oxford, where he subsequently held other research positions before returning to Australia to establish a laboratory at the Florey Institute. He has received various fellowships and awards and is currently Research Co-Lead of the Mental Health Mission, and head of the Epigenetics and Neural Plasticity Laboratory, at the Florey Institute of Neuroscience and Mental Health, University of Melbourne. He is currently Co-Chair of the International Brain Initiative (IBI) Executive, Co-Chair of the Australian Brain Alliance (ABA) Executive, and is a Fellow of the International Behavioral Neuroscience Society (IBNS). Hannan and colleagues provided the first demonstration in any genetic animal model that environmental stimulation can be therapeutic. This has led to new insights into gene-environment interactions in various brain disorders, including Huntington’s disease, dementia, autism, schizophrenia, depression and anxiety disorders. His laboratory at the Florey Institute explores how genes and the environment combine via experience-dependent plasticity in the healthy and diseased brain. Their research includes models of brain disorders which involve cognitive and affective dysfunction, investigated at behavioural, cellular and molecular levels so as to identify pathogenic mechanisms and novel therapeutic targets. This has recently incorporated gut microbiome studies and the microbiota-gut-brain axis. Furthermore, in recent years his group has been exploring transgenerational epigenetic inheritance in response to paternal environmental exposures and experience, and subsequent impacts on offspring brain development, function and dysfunction. This includes discoveries of sperm small and long noncoding RNAs which are modulated by specific environmental exposures, and associated with epigenetic modulation of offspring phenotypes.