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Special lecture held by Liliana Minichiello

Please show up and listen to her interesting ideas entitled: “Understanding the Mechanism of Selective Vulnerability of Striatal Neurons and Its Relevance to Huntington's Disease”. The lecture is hosted by Professor Jørgen Frøkiær, Head of Department for Clinical Medicine

Info about event

Time

Monday 24 June 2024,  at 12:30 - 13:30

Location

at Aarhus University Hospital, Auditorium J116-113

Organizer

Department of Clinical Medicine

Liliana Minichiello, Department of Pharmacology, University of Oxford has been spearheading some exciting breakthroughs in our understanding of Chorea Huntington. She will now come and give her suggestion of how we can progress. Please show up and listen to her interesting ideas entitled:

“Understanding the Mechanism of Selective Vulnerability of Striatal Neurons and Its Relevance to Huntington's Disease”.

It will take place Monday 24 June 2024 at 12:30 – 13:30 at Aarhus University Hospital, Auditorium J116-113, Entrance J110

 

Liliana Minichiello is Academic Research Leader and heading the Laboratory of Cellular and Molecular Neuroscience at the University of Oxford. Liliana has established herself as a world leader in studying the effects of neurotrophins and their receptors on the nervous system, including cognitive function and synaptic plasticity, motor behaviour and metabolism in healthy and neurological conditions. She has a long-standing track record in molecular neuroscience and mouse genetics and has engaged in several excellent collaborations worldwide. Among others, her work aims to elucidate how dysfunctional neurotrophin signalling affects neurological conditions such as Alzheimer’s or Huntington's disease. Importantly, her latest discoveries demonstrate that early in postnatal development, TrkB activation by BDNF in immature hippocampal dentate granule cells (DGCs) provides an instructive signal that drives the sequential maturation of intrinsic hippocampal circuits via the depolarising action of GABA. Disrupting this signal at a critical time when immature DGCs integrate into the hippocampal circuitry leads to neurodevelopmental defects, followed by impairment of synaptic plasticity and cognitive function in adulthood.