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Giovanna Mallucci is a professor in the Department of Clinical Neurosciences at the University of Cambridge. She is a specialist in neurodegenerative diseases and the programme leader in the MRC Toxicology Unit.

Personal History
Professor, Department of Cell Physiology and Pharmacology, University of Leicester 2008 – present

Programme Leader, MRC Toxicology Unit 2008 – present

Consultant Neurologist, National Hospital for Neurology and Neurosurgery 2005 – 2012

Group Leader, MRC Prion Unit 2001-2008

== Qualifications == SciAm 50 Award: ‘Progress against Prions’; for leadership in research, 2007

PhD (London) Neurogenetics, 2000

Training in Internal Medicine and Neurology, 1989-95

MBBS (MD) (London), 1988

BA (Oxon) Physiological Sciences, 1985

Publications
She has a lot of publications which can be found at this link.

Mechanisms of neurotoxicity.
Her background is in modelling prion diseases in mice, looking at mechanisms of neurotoxicity and developing new therapeutic approaches. Her group have shown that early synaptic changes in mice with prion disease can be reversed, resulting in recovery of synaptic and cognitive function and behavioural deficits, long term neuroprotection, and life long survival of affected animals. Thus neurodegeneration can be prevented by reversing early synaptic deficits.

Their program uses several model systems – mice (wild type and transgenic), primary neurons and the nematode C. elegans, to understand the early molecular events that cause synaptic toxicity and neuronal cell death in neurodegeneration. In parallel, they are looking at the mechanisms involved in synaptic repair processes.

Her lab is interested in understanding mechanisms of neurodegeneration. The central theme is the identification of common pathways across the spectrum of these disorders (which include Alzheimer's and related diseases) that are relevant for both mechanistic insights and therapy. They focus both on ‘toxic’ processes that can be targeted to prevent neuronal death, and on regenerative processes that can be harnessed for repair. Using mouse models, they described the pathogenic role of the unfolded protein response (UPR) in neurodegeneration, which led to the discovery of the first small molecule - an inhibitor of this pathway - to prevent neurodegeneration in vivo. They also recently discovered the phenomenon of failure of synaptic repair processes in neurodegeneration and the underlying mechanisms: failure of another stress response involving 'cold shock' proteins, which they have successfully harnessed for neuroprotection. They aim to translate this research for new treatments for dementia.