Elena Di Daniel
Head of Biology
The Biology team in the Alzheimer’s Research UK Oxford Drug Discovery Institute (ODDI) is evaluating novel dementia targets that modulate mechanisms of neuroinflammation and proteostasis.
In vitro cellular assays using disease relevant cells e.g. rodent primary neurons, as well as human iPSC derived neurons and glia are utilized to study a number of targets that have recently emerged from genetic studies in Alzheimer’s disease.
Targets that have potential for drug discovery are prosecuted into screening assays utilizing biochemical or biophysical methods to identify small molecule inhibitors, activators or simply binders to such targets.
We also utilize phenotypic screening approaches. We recently completed a successful phenotypic screening campaign that has identified inhibitors of the NLRP3 inflammasome.
We further test and profile such compound hits, as well as compounds from our target-based screenings, in order to identify the best molecules for progression into drug development.
Recent publications
Microglial inflammation and phagocytosis in Alzheimer's disease: Potential therapeutic targets
Journal article
Nizami S. et al, (2019), British Journal of Pharmacology, 176, 3515 - 3532
A novel high-content imaging-based technique for measuring binding of Dickkopf-1 to low-density lipoprotein receptor-related protein 6
Journal article
Priestley RS. et al, (2019), Journal of Pharmacological and Toxicological Methods, 95, 47 - 55
Targeting SHIP1 for therapeutic intervention in Alzheimer's disease
Conference paper
Mead E. et al, (2019), GLIA, 67, E587 - E588
Development of a high-content imaging-based technique to measure Dickkopf-1 binding to low-density lipoprotein receptor-related protein 6
Conference paper
Priestley RS. et al, (2019), BRITISH JOURNAL OF PHARMACOLOGY, 176, 2990 - 2990
Oscillating Magnet Array−Based Nanomagnetic Gene Transfection: A Valuable Tool for Molecular Neurobiology Studies
Journal article
Subramanian M. et al, (2017), Nanomaterials, 7, 28 - 28
bnormalities in α/β-CaMKII and related mechanisms suggest synaptic dysfunction in hippocampus of LPA1 receptor knockout mice
Journal article
Musazzi L. et al, (2011), The International Journal of Neuropsychopharmacology, 14, 941 - 953
Evaluation of expression and function of the H+/myo-inositol transporter HMIT
Journal article
Di Daniel E. et al, (2009), BMC Cell Biology, 10
Neural network dysfunction in bipolar depression: clues from the efficacy of lamotrigine
Journal article
Large CH. et al, (2009), Biochemical Society Transactions, 37, 1080 - 1084
Investigation of the H+–myo-inositol transporter (HMIT) as a neuronal regulator of phosphoinositide signalling
Journal article
Daniel ED. et al, (2009), Biochemical Society Transactions, 37, 1139 - 1143
Prolyl oligopeptidase binds to GAP-43 and functions without its peptidase activity
Journal article
Di Daniel E. et al, (2009), Molecular and Cellular Neuroscience, 41, 373 - 382
P.1.g.010 Regulation of neuronal growth cone morphology by prolyl oligopeptidase revealed by manipulation of gene expression
Conference paper
Di Daniel E. et al, (2007), European Neuropsychopharmacology, 17, S308 - S308
The common inositol-reversible effect of mood stabilizers on neurons does not involve GSK3 inhibition, myo-inositol-1-phosphate synthase or the sodium-dependent myo-inositol transporters
Journal article
Di Daniel E. et al, (2006), Molecular and Cellular Neuroscience, 32, 27 - 36
nalysis of prolyl oligopeptidase (PO) as a target for bipolar disorder — characterisation of PO null-mutant mice
Conference paper
Di Daniel E. et al, (2006), European Neuropsychopharmacology, 16, S22 - S23
potential mechanism for the action of mood stabilizers involves prolyl oligopeptidase and its interaction with growth-associated protein
Conference paper
Di Daniel E. et al, (2006), BIPOLAR DISORDERS, 8, 61 - 61
Serotonin transporter gene polymorphism (5-HTTLPR) and emotional response to auditory hallucinations in schizophrenia
Conference paper
Sanjuan J. et al, (2005), The International Journal of Neuropsychopharmacology, 9, 131 - 131
Comparative analysis of the effects of four mood stabilizers in SH‐SY5Y cells and in primary neurons
Journal article
Daniel ED. et al, (2005), Bipolar Disorders, 7, 33 - 41
Behavioural and neurochemical profiling of prolyl oligopeptidase knock-out mice
Conference paper
Rourke C. et al, (2005), JOURNAL OF PSYCHOPHARMACOLOGY, 19, A51 - A51
Expression and Characterization of GSK-3 Mutants and Their Effect on β-Catenin Phosphorylation in Intact Cells
Journal article
Hagen T. et al, (2002), Journal of Biological Chemistry, 277, 23330 - 23335
Phenotypic Knockout of Nerve Growth Factor in Adult Transgenic Mice Reveals Severe Deficits in Basal Forebrain Cholinergic Neurons, Cell Death in the Spleen, and Skeletal Muscle Dystrophy
Journal article
Ruberti F. et al, (2000), The Journal of Neuroscience, 20, 2589 - 2601
Muscular dystrophy in adult and aged anti-NGF transgenic mice resembles an inclusion body myopathy
Journal article
Capsoni S. et al, (2000), Journal of Neuroscience Research, 59, 553 - 560
In vitro down regulation of ICAM-1 and E-cadherin and in vivo reduction of lung metastases of TS/A adenocarcinoma by a lysozyme derivative.
Journal article
Pacor S. et al, (1999), International journal of molecular medicine, 4, 369 - 375