University of Dundee

"Modulating the UPR for treatment of neurodegenerative disease"

Event Date: 
Tuesday, September 18, 2018 - 16:00 to 17:00
Event Location: 
MSI Small Lecture Theatre
Host: 
Professor Miratul Muqit
Event Speaker: 
Professor Giovanna Mallucci
Institution: 
UK Dementia Research Institute, University of Cambridge
Event Type: 
Seminar
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Biography:

 Giovanna Mallucci is Associate Director of the UK Dementia Research Institute (UK DRI) at the University of Cambridge, van Geest Professor of Clinical Neurosciences and an Honorary Consultant Neurologist at Addenbrooke’s Hospital, specialising in Dementia. Her undergraduate degrees were in Physiological Sciences and Medicine from the University of Oxford, with clinical training at University College, London. She obtained her PhD from London University in Neurogenetics,for which she generated a mouse model that paved the way to her discoveries about reversibility of early neurodegeneration and underlying mechanisms. Since her PhD she has combined clinical work and basic research and led groups in the MRC Prion Unit (2001-2008) and the MRC Toxicology Unit (2008-2018) at the University of Leicester, before moving to Cambridge. She has received numerous national and international awards for her innovators worldwide. In 2017, she was elected Fellow of the Academy of Medical Sciences.

 

Research Interests:

 Professor Mallucci’s lab is internationally recognised for landmark studies defining common mechanisms underlying the causes of dementia and other neurodegenerative disorders, like Parkinson’s disease, which can be targeted for treatment. It is in this area, of modulating pathways involved in neurodegeneration, that a team led by Prof Mallucci recently made a major breakthrough. After screening over 1000 safe and mostly licensed drugs, they identified two compounds, trazodone hydrochloride (a drug used to treat depression), and dibenzoylmethane (a compound being trialled as an anti-cancer drug), that prevented the emergence of brain cell damage and restored memory in both prion-diseased mice and in mice with frontotemporal dementia. Critically, the drugs reduced brain cell death and brain shrinkage – a feature of neurodegenerative diseases, and prolonged survival. We currently have no way of treating these diseases, so the prospect of finding drugs that can slow or stop them from progressing is extremely exciting. This is especially true when this is based on drugs that are known to be safe in humans, and in particular the elderly, avoiding the need for highly expensive and timeconsuming testing to establish safety.