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Prof Karen Duff
Cruciform Building
Gower Street
London
WC1E 6BT
Prof Karen Duff profile picture
Appointment
  • UK DRI Associate Director (Professor in Dementia and Neurodegeneration)
  • UK Dementia Research Institute
  • UCL Queen Square Institute of Neurology
  • Faculty of Brain Sciences
Biography
After receiving my Ph.D from Sydney Brenner’s department at the University of Cambridge in 1991 I undertook postdoc positions in London with Alison Goate (1991-92) and John Hardy at the University of South Florida (1992-94). I was an Assistant Professor at the University of South Florida (1993-1996), Associate Professor at Mayo Clinic Jacksonville (1996-1998), and Professor at the New York University Nathan Kline Institute (1998-2006) followed by Columbia University (2006-2019) where I was deputy director of the Taub Institute.

Over the last 27 years, I have created several transgenic mouse models for Alzheimer’s disease, FTD and other dementias to explore disease mechanisms and test therapeutic approaches. My current interests are in exploring the role of the risk factor ApoE4 in AD pathogenesis, exploring the mechanisms and circuitry involved in the spread of pathogenic proteins within the brain and identifying the role and therapeutic potential of autophagy and proteasome-mediated clearance to remove pathological proteins.
Research Summary
Alzheimer’s disease is characterised by the accumulation of protein clumps in the brain, a loss of neurons and memory decline. Over the past decade, it has emerged that one of these harmful proteins, tau, spreads across the brain from neuron to neuron, in a predictable pattern as the disease progresses. Previous research from Prof Karen Duff and her team has explored this phenomenon in great detail. As part of her new programme at UK DRI and using a series of sophisticated methods, she hopes to find ways in which to stop this spreading and slow disease development.

The Duff lab additionally aims to investigate other key questions in dementia research including why the accumulation of abnormal tau protein leads to many different types of disease, why certain neurons are more vulnerable than others to the harmful effects of tau, how we can help to clear these proteins out of the brain and whether genetic risk factors can give us greater insight into the biological mechanisms behind Alzheimer’s disease and Frontotemporal dementia-tau. It is the hope that deeper understanding in these research areas will drive the development of therapeutics for people living with dementia.
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