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Partner 14: Lancaster University (ULANC), United Kingdom
Scientist responsible: Prof. David Allsop
Brief description of our organization
Lancaster University is home to over 2,500 staff and 16,500 students and is consistently ranked as the best university in the North West of England. We are located in the Division of Biomedical and Life Sciences, which is part of the newly formed School of Health and Medicine (SHM), which offers a diverse range of undergraduate and postgraduate taught and research programmes in biology, biomedicine, medicine and the social aspects of health. Key areas of research in SHM include the study of end-of-life care, disability, mental health, epidemiology, cancer biology, neurodegenerative diseases, immunology and microbiology.
Our research group are studying the role of protein aggregates in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, prion disease, frontotemporal dementia and motor neuron disease, as well as late-onset diabetes mellitus. We are involved in three main areas of research: (1) the potential links between protein aggregation and cell death, and particularly the role that redox-active metal ions and free radicals might play in the this process; (2) certain key proteins in blood plasma and cerebrospinal fluid as potential biomarkers for the onset or progression of protein aggregation diseases; and (3) aggregation inhibitors as novel therapeutics.
Our research is supported by The Alzheimer’s Society; The Medical Research Council; The European Community; The Fisher Foundation; and The George Barton Trust.
Current members of our research team are:
Prof. David Allsop
Dr. Susan Moore
Dr. Brian Tabner
Dr. Tom Huckerby
Dr. Penelope Foulds
Jenny Mayes
Lee Hayes
Kirsty Humphreys
Kath Lamb
Some of our recent publications
Tabner B.J., Turnbull S., El-Agnaf O.M.A. & Allsop D. (2002) Formation of hydrogen peroxide and hydroxyl radicals from Aβ and α-synuclein as a possible mechanism of cell death in Alzheimer’s disease and Parkinson’s disease. Free Radical Biol. Med. 32, 1076-1083.
Moore S.A., Huckerby T.N., Gibson G.L., Fullwood N.J., Turnbull S., Tabner B.J., El-Agnaf O.M.A. & Allsop D. (2004) Both the D-(+) and L-(-) enantiomers of nicotine inhibit Aβ aggregation and cytotoxicity. Biochemistry 43, 819-826.
Tabner B.J., El-Agnaf O.M.A., Turnbull S., German M.J., Paleologou K.E., Hayashi Y., Cooper L.J., Fullwood N.J. & Allsop D. (2005) Hydrogen peroxide is generated during the very early stages of aggregation of the amyloid peptides implicated in Alzheimer's disease and familial British dementia. J. Biol. Chem. 280, 35789-35792 .
El-Agnaf O.M.A., Salem S.A., Paleologou K.E., Curran M.D., Gibson M.J., Court J.A., Schlossmacher M.G. & Allsop D. (2006) Detection of oligomeric forms of α-synuclein protein in human plasma as a potential biomarker for Parkinson’s disease. FASEB J. 20, 419-425.
Tokuda T., Salem S., Allsop D., Mizuno T., Nakagawa M., Qureshi M.M., Locascio J.J., Schlossmacher M.G. & El-Agnaf, O.M.A. (2006) Decreased α-synuclein in cerebrospinal fluid of aged individuals and subjects with Parkinson's disease. Biochem. Biophys. Res. Commun. 349, 162-166.
Masad A., Hayes L., Tabner B.J, Turnbull S., Cooper L.J., Fullwood N.J., German M.J., Kametani F., El Agnaf O.M.A. & Allsop D. (2007) Copper-mediated formation of hydrogen peroxide from the amylin peptide: a novel mechanism for degeneration of islet cells in type-2 diabetes mellitus? FEBS Letts. 581, 3489-3493.
Austen B.M., Paleologou K.E., Sumaya A., Ali E., Qureshi M.M., Allsop D. & El-Agnaf O.M.A. (2008) Designing peptide inhibitors for oligomerization and toxicity of Alzheimer’s β-amyloid peptide. Biochemistry 47, 1984-1992.
Allsop D., Mayes J., Moore S., Masad A. & Tabner B. (2008) Metal-dependent generation of reactive oxygen species from amyloid proteins implicated in neurodegenerative disease. Biochem. Soc. Trans. 36, 1293-1298.
Foulds P., McAuley E., Gibbons L., Davidson Y., Pickering-Brown S.M., Neary D., Snowden J.S., Allsop D. & Mann D.M.A. (2008) TDP-43 protein can be detected in plasma in patients with Alzheimer’s disease and frontotemporal dementia and may witness the presence of TDP-43 pathology within the brain. Acta Neuropathol. 116, 141-146.
Paleologou K.E., Salem S.A., Al-Shami R., Mann D.M.A., Allsop D., Ali S.A.E., Hassan A.H., Petersen C.L., Jensen P.H. & El-Agnaf O.M.A. (2009) FILA-1 antibody detects elevated levels of soluble α-synuclein oligomers in brain extracts from patients with dementia with Lewy bodies. Brain (in press).
Kasaia T., Tokuda T., Ishigamia, N., Sasayama H., Foulds P., Mitchell J.D., Mann D.M.A., Allsop D. & Nakagawa M. (2009) Increased TDP-43 protein in cerebrospinal fluid of patients with amyotrophic lateral sclerosis. Acta Neuropathol. 117, 1293-1298.
Matharu B., Gibson G.R., Parsons, R.B., Huckerby T.N., Moore S., Cooper, L.J., Allsop D. & Austen B. (2009) Galantamine inhibits β-amyloid aggregation and cytotoxicity. J. Neurol. Sci. (in press).
Links
http://www.lancs.ac.uk/aboutLU/index.htm
http://www.lancs.ac.uk/shm/
http://www.lancs.ac.uk/shm/people/david-allsop/bls/
http://www.biochemistry.org/meetings/programme.cfm?Meeting_No=SA078
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