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Brief Communication

Ceruloplasmin dysfunction and therapeutic potential for parkinson disease

  1. Scott Ayton PhD1,
  2. Peng Lei PhD1,
  3. James A. Duce PhD1,
  4. Bruce X. W. Wong PhD1,
  5. Amelia Sedjahtera BBMS(Hons)1,
  6. Paul A. Adlard PhD2,3,
  7. Ashley I. Bush MBBS, PhD1,3,*,
  8. David I. Finkelstein PhD1,2

Article first published online: 19 FEB 2013

DOI: 10.1002/ana.23817

Additional Information

How to Cite

Ayton, S., Lei, P., Duce, J. A., Wong, B. X. W., Sedjahtera, A., Adlard, P. A., Bush, A. I. and Finkelstein, D. I. (2013), Ceruloplasmin dysfunction and therapeutic potential for parkinson disease. Ann Neurol.. doi: 10.1002/ana.23817

Author Information

  1. 1

    Oxidation Biology Laboratory, Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia

  2. 2

    Synaptic Neurobiology, Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia

  3. 3

    Department of Pathology, University of Melbourne, Parkville, Victoria, Australia

*Address correspondence to Dr Bush, Florey Institute of Neuroscience and Mental Health, 30 Royal Parade, University of Melbourne, Victoria 3010, Australia. E-mail: ashleyib@unimelb.edu.au

Publication History

  1. Article first published online: 19 FEB 2013
  2. Accepted manuscript online: 24 NOV 2012 04:54AM EST
  3. Manuscript Accepted: 16 NOV 2012
  4. Manuscript Revised: 16 OCT 2012
  5. Manuscript Received: 16 APR 2012

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Ceruloplasmin is an iron-export ferroxidase that is abundant in plasma and also expressed in glia. We found a ∼80% loss of ceruloplasmin ferroxidase activity in the substantia nigra of idiopathic Parkinson disease (PD) cases, which could contribute to the pro-oxidant iron accumulation that characterizes the pathology. Consistent with a role for ceruloplasmin in PD etiopathogenesis, ceruloplasmin knockout mice developed parkinsonism that was rescued by iron chelation. Additionally, peripheral infusion of ceruloplasmin attenuated neurodegeneration and nigral iron elevation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model for PD. These findings show, in principle, that intravenous ceruloplasmin may have therapeutic potential in PD. Ann Neurol 2013

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