Dr Charles Harrington
BSc (Hons) (Glasgow, 1977); PhD (Glasgow, 1980)
Senior Research Fellow
Charlie Harrington graduated in Microbiology from Glasgow University where he developed an interest in chemical microbiology and the study of microbial cell walls. He completed his PhD working with Dr Julia Douglas on cell wall synthesis in yeast and followed with a one-year NIH-funded Fellowship with Dr Wilf Arnold in Kansas City, Missouri studying enzymes within the yeast cell envelope. After this, Charlie joined Professor Sir James Baddiley in the Department of Biochemistry at the University of Cambridge as a Research Fellow, where he spent four years investigating the synthesis of bacterial cell wall polymers. Dr Harrington then spent over two years at Murex Medical Research Ltd., Cambridge, developing diagnostic tests for microbial diseases, including methicillin-resistant Staphylococcus aureus and sexually transmitted diseases. This combined monoclonal antibody technology with his knowledge of the microbial cell surface.
In 1988, he joined Claude Wischik working at the Medical Research Council’s Laboratory of Molecular Biology. Working in the Cambridge Brain Bank Laboratory over a period of 10 years. During this time, Wischik, Harrington and colleagues developed an assay for screening agents having the potential to prevent the tau pathology that is the hallmark of Alzheimer’s disease. Charlie moved with Professor Wischik, in 1998, to the University of Aberdeen, where he was appointed as a Senior Research Fellow.
The Alzheimer's research was translated to the clinic, through a spin-out company, TauRx Therapeutics, who are conducting phase 3 trials of hydromethylthionine. Dr Harrington is Chief Scientific Officer for TauRx Therapeutics Ltd responsible for the non-clinical activities of the company.
- BSc (Hons) Microbiology1977 - University of Glasgow
- PhD Microbiology1980 - University of Glasgow
Proteomic analysis of hydromethylthionine in the line 66 model of frontotemporal dementia demonstrates actions on tau-dependent and tau-independent networksCells, vol. 10, no. 8, 2162Contributions to Journals: Articles
Degeneration of basal and limbic networks is a core feature of behavioural variant frontotemporal dementiaBrain CommunicationsContributions to Journals: Articles
Tau Protein Phosphorylated at Threonine-231 Is Expressed Abundantly in the Cerebellum in Prion EncephalopathiesJournal of Alzheimer's Disease, vol. 81, no. 2, pp. 769-785Contributions to Journals: Articles
Elucidating the neuropathologic mechanisms of SARS-CoV-2 infectionFrontiers in Neurology, vol. 12, 660087Contributions to Journals: Articles
Insoluble Vascular Amyloid Deposits Trigger Disruption of the Neurovascular Unit in Alzheimer’s Disease BrainsInternational Journal of Molecular Sciences, vol. 22, no. 7, 3654Contributions to Journals: Articles
Dr Harrington has research interests in the neurodegenerative diseases and, in particular, Alzheimer’s disease. His main focus has been on the biology of tau protein in aging and in Alzheimer’s disease. Dr Harrington’s research is aimed at diseases that are characterised by protein aggregation and methods by which these processes might be prevented.
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Assays for the Screening and Characterization of Tau Aggregation InhibitorsTau Protein. Smet-Nocca, C. (ed.). Springer, pp. 129-140, 12 pagesChapters in Books, Reports and Conference Proceedings: Chapters
Efficacy and safety of tau-aggregation inhibitor therapy in patients with mild or moderate Alzheimer's disease: a randomised, controlled, double-blind, parallel-arm, phase 3 trialThe Lancet, vol. 388, no. 10062, pp. 2873-2884Contributions to Journals: Articles
Inhibition of Tau Aggregation as a Basis for Treatment and Prevention of Alzheimer's DiseaseDeveloping Therapeutics for Alzheimer's Disease. Wolfe, M. S. (ed.). Elsevier Inc., pp. 385-436, 52 pagesChapters in Books, Reports and Conference Proceedings: Chapters
Absence of a Role for Phosphorylation in the Tau Pathology of Alzheimer's DiseaseBiomolecules, vol. 6, no. 2, pp. 1-19Contributions to Journals: Articles
Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective StrategiesBiomolecules, vol. 6, no. 1, 6Contributions to Journals: Review articles
Different pathways of molecular pathophysiology underlie cognitive and motor tauopathy phenotypes in transgenic models for Alzheimer’s disease and frontotemporal lobar degenerationCellular and Molecular Life Sciences, vol. 72, no. 11, pp. 2199-2222Contributions to Journals: Articles
Effects of oxidized and reduced forms of methylthioninium in two transgenic mouse tauopathy modelsBehavioural Pharmacology, vol. 26, no. 4, pp. 353-368Contributions to Journals: Articles
Cellular Models of Aggregation-Dependent Template-Directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer's DiseaseThe Journal of Biological Chemistry, vol. 290, no. 17, pp. 10862-10875Contributions to Journals: Articles
The relationship between truncation and phosphorylation at the C-terminus of tau protein in the paired helical filaments of Alzheimer's diseaseFrontiers in Neuroscience, vol. 9, 33Contributions to Journals: Articles
Tau Aggregation Inhibitor Therapy: An Exploratory Phase 2 Study in Mild or Moderate Alzheimer's DiseaseJournal of Alzheimer's Disease, vol. 44, no. 2, pp. 705-720Contributions to Journals: Articles