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James W. Ironside

Researcher at University of Edinburgh

Publications -  592
Citations -  35714

James W. Ironside is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Bovine spongiform encephalopathy & PRNP. The author has an hindex of 86, co-authored 590 publications receiving 33745 citations. Previous affiliations of James W. Ironside include St Mary's Hospital & Western General Hospital.

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A new variant of Creutzfeldt-Jakob disease in the UK

TL;DR: Ten cases of Creutzfeldt-Jakob disease have been identified in the UK in recent months with a new neuropathological profile that raises the possibility that they are causally linked to BSE.
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Transmissions to mice indicate that ‘new variant’ CJD is caused by the BSE agent

TL;DR: It is shown that the strain of agent from cattle affected by bovine spongiform encephalopathy (BSE) produces a characteristic pattern of disease in mice that is retained after experimental passage through a variety of intermediate species, providing strong evidence that the same agent strain is involved in both BSE and vCJD.
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Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD

TL;DR: Strain characteristics revealed here suggest that the prion protein may itself encode disease phenotype, consistent with BSE being the source of this new disease.
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Investigation of variant Creutzfeldt-Jakob disease and other human prion diseases with tonsil biopsy samples

TL;DR: If, in the appropriate clinical context, a tonsil biopsy sample was positive for PrPSc, variant CJD could be diagnosed, which obviates the need for a brainBiopsy sample to be taken, and the results show that variants CJD has a different pathogenesis to sporadic CJD.
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Compelling transgenetic evidence for transmission of bovine spongiform encephalopathy prions to humans.

TL;DR: It is reported that transgenic (Tg) mice expressing bovine (Bo) prion protein (PrP) serially propagate BSE prions and that there is no species barrier for transmission from cattle to Tg(Bo PrP) mice.