- Identification of bioactive metabolites in human iPSC-derived dopaminergic neurons with PARK2 mutation: Altered mitochondrial and energy metabolism 28 May 2021 Justyna Okarmus
- Geographical distribution of fertility rates in 70 low-income, lower-middle-income, and upper-middle-income countries, 2010-16: a subnational analysis of cross-sectional surveys 21 May 2021 Carla Pezzulo
- Gene therapy restores dopamine transporter expression and ameliorates pathology in iPSC and mouse models of infantile parkinsonism 20 May 2021 Joanne Ng
- Non-neuronal cells in amyotrophic lateral sclerosis - from pathogenesis to biomarkers 30 April 2021 Björn F Vahsen
- Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infection of lung epithelial cells 14 April 2021 Peter A C Wing
- The antigenic anatomy of SARS-CoV-2 receptor binding domain 23 March 2021 Wanwisa Dejnirattisai
- Reduced neutralization of SARS-CoV-2 B.1.1.7 variant by convalescent and vaccine sera 21 March 2021 Piyada Supasa
- Evidence of escape of SARS-CoV-2 variant B.1.351 from natural and vaccine-induced sera 17 March 2021 Daming Zhou
- In vitro Quantitative Imaging Assay for Phagocytosis of Dead Neuroblastoma Cells by iPSC-Macrophages 1 March 2021 Hazel Hall-Roberts
- Breadth and function of antibody response to acute SARS-CoV-2 infection in humans 26 February 2021 Kuan-Ying A Huang
Postdoctoral Research Assistant | ARUK ODDI | email@example.com
Dr Hazel Hall-Roberts (née Roberts) joined the lab in 2016, to research the role of microglia in Alzheimer’s disease. Microglia are immune cells that maintain a healthy brain environment by clearing up pathogens and ‘self’-made debris through a process called phagocytosis (‘cell eating’). Pathogens provoke a fuIl immune response, but ‘self’ debris usually does not. In an Alzheimer’s brain, microglial phagocytosis is impaired, and the microglia enter a state of chronic inflammation, in the absence of pathogens. Hazel’s current project is jointly supervised by Dr Sally Cowley, and Dr Elena Di Daniel at the Alzheimer’s Research UK Oxford Drug Discovery Institute. Their main goal is to develop assays and tools for investigating microglial function in the context of Alzheimer’s disease, particularly their ability to clear neuronal debris via phagocytosis, using iPSC-derived macrophages as a cell model.
Hazel graduated from the University of Bristol in 2012 with a BSc in Biochemistry with Year in Industry, having spent a year working at GlaxoSmithKline Stevenage. At GlaxoSmithKline her research project looked at epigenetic proteins involved in the acute inflammation response of macrophages. This was followed by a PhD at the University of Bath (2012-16) with Professor David Brown, conducting research on α-synuclein, a protein that disrupts cell function in Parkinson’s disease, and how it promotes neuronal cell secretion of β-amyloid, a peptide that plays a key role in Alzheimer’s disease.