Journal article
Manganese chelation therapy extends survival in a mouse model of M1000 prion disease
MW Brazier, I Volitakis, M Kvasnicka, AR White, JR Underwood, JE Green, S Han, AF Hill, CL Masters, SJ Collins
Journal of Neurochemistry | WILEY | Published : 2010
Abstract
Previous in vitro and in vivo investigations have suggested manganese (Mn2+) may play a role in pathogenesis through facilitating refolding of the normal cellular form of the prion protein into protease resistant, pathogenic isoforms (PrPSc), as well as the subsequent promotion of higher order aggregation of these abnormal conformers. To further explore the role of Mn2+ in pathogenesis, we undertook a number of studies, including an assessment of the disease modifying effects of chelation therapy in a well-characterized mouse model of prion disease. The di-sodium, calcium derivative of the chelator, cyclohexanediaminetetraacetic acid (Na 2CaCDTA), was administered intraperitoneally to mice i..
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Grants
Awarded by National Health and Medical Research Council (NHMRC)
Funding Acknowledgements
The authors thank the Animal Housing Facility staff in the Faculty of Medicine, Dentistry and Health Sciences, the University of Melbourne for their assistance with animal husbandry.SJ Collins, AR White, AF Hill and CL Masters receive support from a National Health and Medical Research Council (NHMRC) Program Grant # 400202. SJ Collins is a recipient of an NHMRC Practitioner Fellowship # 400183. AF Hill is the recipient of an NHMRC RD Wright Career Development Award. The Australian National CJD Registry is funded by the Commonwealth Department of Health and Ageing. The anti-prion protein monoclonal antibody ICSM18 was a generous gift from Professor John Collinge.