After receiving a MSc in Bioengineering (SupAgro, 2007) and a MRes in Biomedical Research (Imperial College, 2007), Mattéa completed her DPhil in neurosciences at the University of Oxford (2010) in Prof Dame Kay Davies' group. She did her first postdoc at Mount Sinai School of Medicine, New York (2011-2013) in Dr Jenny Zou's laboratory where she investigated axonal regeneration after spinal cord injury. For her second postdoc (2013-2018) in Prof Peter Oliver's group at the University of Oxford, she studied a novel family of neuroprotective proteins implicated in the oxidative stress response. She then joined Prof Kevin Talbot's and Prof Martin Turner's groups (University of Oxford, 2018-2019) as a visiting researcher where she gained further expertise in stem cell technology and novel proteomic approaches.
As an Anne McLaren Fellow, Mattéa started her own independent research group at the University of Nottingham in January 2020. She was awarded an Alzheimer's Disease Research UK Midlands Pump-priming Award and a Royal Society Research Grant in 2021.
Since her DPhil, Mattéa has been exploring the multiple facets of the neurodegenerative process and has acquired expertise in a wide range of molecular and cellular approaches, animal models, as well as in transcriptomics, metabolomics and proteomics. Her main research focus centers around the role of oxidative and nitrosative stresses and redox mechanisms in the pathophysiology of neurodegenerative conditions.
The long-term goal of the Finelli group is to understand how redox mechanisms contribute to the progressive dysfunction and death of neurons in neurodegenerative conditions, such as dementia, and to… read more
CASTROFLORIO E, DEN HOED J, SVISTUNOVA D, FINELLI MJ, CEBRIAN-SERRANO A, CORROCHANO S, BASSETT AR and DAVIES B, 2021. The Ncoa7 locus regulates V-ATPase formation and function, neurodevelopment and behaviour. Cell Mol Life Sci.. 78(7), 3503-3524 EMILY FENEBERG, DAVID GORDON, ALEXANDER G THOMPSON, MATTÉA J FINELLI, RUXANDRA DAFINCA, ANA CANDALIJA, PHILIP D CHARLES, IMRE MÄGER, MATTHEW J WOOD, ROMAN FISCHER, BENEDIKT M KESSLER, ELIZABETH GRAY, MARTIN R TURNER and KEVIN TALBOT, 2020. An ALS-linked mutation in TDP-43 disrupts normal protein interactions in the motor neuron response to oxidative stress Neurobiol Dis..
EMILY FENEBERG, PHILIP D CHARLES, MATTÉA J FINELLI, CONNOR SCOTT, BENEDIKT M KESSLER, ROMAN FISCHER, OLAF ANSORGE, ELIZABETH GRAY, KEVIN TALBOT and MARTIN R TURNER, 2020. Detection and Quantification of Novel C-terminal TDP-43 Fragments in ALS-TDP
The long-term goal of the Finelli group is to understand how redox mechanisms contribute to the progressive dysfunction and death of neurons in neurodegenerative conditions, such as dementia, and to translate the findings from basic research into new therapeutic strategies for these diseases. In particular, we explore how oxidative and nitrosative (O/N) stresses regulate cell-cell communication in normal brain physiology, aging and dementia.
The main aims of our group are (i) to identify the signaling proteins that are modified by O/N stresses in dementia, (ii) understand how dementia-associated redox-modified proteins can elicit transduction of a faulty signaling in target cells leading to dysfunction and degeneration of these cells and (iii) explore whether redox-modified proteins could be used as a diagnostic/prognostic tool for various forms/stages of dementia.
As disease-relevant model system, we use glial and neuronal cells differentiated from stem cells reprogrammed from skin biopsies of controls or patients with neurodegenerative conditions. We use a combination of state-of-the-art redox and quantitative proteomics, as well as a wide range of cell- and recombinant protein-based functional assays.