Iron in Central Nervous System Disorders

1. Front Matter

   Pages I-VII

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2. Cellular and regional maintenance of iron homeostasis in the brain: normal and diseased states

   • J. R. Connor

   Pages 1-18

3. Iron deposits in brain disorders

   • K. Jellinger, E. Kienzl

   Pages 19-36

4. Brain iron and schizophrenia

   • K. W. Lange, J. Kornhuber, P. Kruzik, W.-D. Rausch, E. Gabriel, K. Jellinger et al.

   Pages 37-43

5. Some reflections on iron dependent free radical damage in the central nervous system

   • M. E. Götz, A. Dirr, W. Gsell, R. Burger, A. Freyberger, P. Riederer

   Pages 45-54

6. Iron regulation of dopaminergic transmission: relevance to movement disorders

   • D. Ben-Shachar, A. Tovi, M. B. H. Youdim

   Pages 55-66

7. Dopaminergic cell death in Parkinson’s disease: a role of iron?

   • F. Javoy-Agid, B. Faucheux

   Pages 67-77

8. Iron and neurotoxin intoxication: comparative in vitro and in vivo studies

   • W. Wesemann, St. Blaschke, H.-W. Clement, Chr. Grote, N. Weiner, W. Kolasiewicz et al.

   Pages 79-86

9. Intranigral iron infusion in rats: A progressive model for excess nigral iron levels in Parkinson’s disease?

   • G. W. Arendash, C. W. Olanow, G. J. Sengstock

   Pages 87-101

10. Iron storage and transport markers in Parkinson’s disease and MPTP-treated mice

    • D. C. Mash, J. Singer, J. Pablo, M. Basile, J. Bruce, W. J. Weiner

    Pages 103-116

11. Pathogenesis of Parkinson’s disease: iron and mitochondrial DNA deletion

    • Y. Mizuno, H. Mochizuki, K. Nishi, S.-i. Ikebe, N. Hattori, Y. Hattori-Nakagawa

    Pages 117-135

12. Consequences of intrastriatally administrated FeCl3 and 6-OHDA without and after transient cerebral oligemia on behaviour and navigation

    • C. Heim, W. Kolasiewicz, T. Jaros, K.-H. Sontag

    Pages 137-153

13. Cytokine induced synthesis of nitric oxide from L-arginine: a cytotoxic mechanism that targets intracellular iron

    • J. B. Hibbs Jr.

    Pages 155-171

14. Lazaroids: potent inhibitors of iron-dependent lipid peroxidation for neurodegenerative disorders

    • E. D. Hall, J. M. McCall

    Pages 173-188

15. The treatment of iron overload — psychiatric implications

    • M. Struck, P. Waldmeier, V. Berdoukas

    Pages 189-196

16. Iron therapy: Pros and Cons

    • G. Stern

    Pages 197-202

17. Back Matter

    Pages 203-208

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The role of the metals copper, zinc, magnesium, lead, manganese, mercury, lithium and aluminium in neuropsychiatric disease are well known and has been discussed on several occasions. Yet little attention has been paid to iron, the most abundant transitional metal in the body and the earth's crust. Iron plays a major role as a cofactor of numerous metabolic enzymes, it is important for DNA and protein synthesis, and has a crucial role in the oxygen carrying capacity of haemoglobin. Some of the most devastating diseases of systemic organs are associated with abnormal iron metabolism. Yet only very recently its role in the central nervous system has been considered. Thus nutritional iron defi­ ciency and iron overload afflict some 500-600 million people. It is also well recognized that too little or too much iron can produce profound effects on the metabolic state of the cell, and therefore the regulation of iron uptake and disposition is tightly relegated by the cell. Its transport into the cell and storage are handled by transferrin, ferritin and haemo­ siderin. Nowhere are these processes so well recognized as in the case of brain iron metabolism. Iron does not have ready access to the adult brain as it does to other tissues, since it does not cross the blood brain barrier (BBB). All the iron present in brain is deposited before the closure of BBB at an early age where it is sequestered and conserved. Therefore its turnover is extremely slow.

• Central Nervous System
• DNA
• Lipid
• Nervous System
• Oxidation
• Parkinson
• dopamine

• Department of Psychiatry, University of Würzburg, Federal Republic of Germany

  Peter Riederer

• Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel

  M. B. H. Youdim

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