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Genetic or pharmacological iron chelation prevents MPTP-induced neurotoxicity in vivo: a novel therapy for Parkinson's disease.

Studies on postmortem brains from Parkinson's patients reveal elevated iron in the substantia nigra (SN). Selective cell death in this brain region is associated with oxidative stress, which may be exacerbated by the presence of excess iron. Whether iron plays a causative role in cell death, however, is controversial. Here, we explore the effects of iron chelation via either transgenic expression of the iron binding protein ferritin or oral administration of the bioavailable metal chelator clioquinol (CQ) on susceptibility to the Parkinson's-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrapyridine (MPTP). Reduction in reactive iron by either genetic or pharmacological means was found to be well tolerated in animals in our studies and to result in protection against the toxin, suggesting that iron chelation may be an effective therapy for prevention and treatment of the disease.

Pubmed ID: 12670420

Authors

  • Kaur D
  • Yantiri F
  • Rajagopalan S
  • Kumar J
  • Mo JQ
  • Boonplueang R
  • Viswanath V
  • Jacobs R
  • Yang L
  • Beal MF
  • DiMonte D
  • Volitaskis I
  • Ellerby L
  • Cherny RA
  • Bush AI
  • Andersen JK

Journal

Neuron

Publication Data

March 27, 2003

Associated Grants

  • Agency: NIA NIH HHS, Id: 2R01AG12686
  • Agency: NIA NIH HHS, Id: R01 AG12141
  • Agency: NIA NIH HHS, Id: R01 AG41264

Mesh Terms

  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
  • 3,4-Dihydroxyphenylacetic Acid
  • Animals
  • Blotting, Western
  • Cell Death
  • Clioquinol
  • Dopamine
  • Ferritins
  • Gene Expression
  • Genetic Therapy
  • Homovanillic Acid
  • Humans
  • Immunohistochemistry
  • Iron
  • Iron Chelating Agents
  • Mice
  • Mice, Transgenic
  • Oxidative Stress
  • Parkinson Disease
  • Parkinson Disease, Secondary
  • Promoter Regions, Genetic
  • Rats
  • Substantia Nigra
  • Tyrosine 3-Monooxygenase