Iron in Central Nervous System Disorders

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 cr...

Full description

Bibliographic Details
Other Authors: Riederer, Peter (Editor), Youdim, M.B.H. (Editor)
Format: eBook
Language:English
Published: Vienna Springer Vienna 1993, 1993
Edition:1st ed. 1993
Series:Key Topics in Brain Research
Subjects:
Online Access:
Collection: Springer Book Archives -2004 - Collection details see MPG.ReNa
LEADER 03760nmm a2200349 u 4500
001 EB000709417
003 EBX01000000000000000562499
005 00000000000000.0
007 cr|||||||||||||||||||||
008 140122 ||| eng
020 |a 9783709193228 
100 1 |a Riederer, Peter  |e [editor] 
245 0 0 |a Iron in Central Nervous System Disorders  |h Elektronische Ressource  |c edited by Peter Riederer, M.B.H. Youdim 
250 |a 1st ed. 1993 
260 |a Vienna  |b Springer Vienna  |c 1993, 1993 
300 |a VII, 205 p  |b online resource 
505 0 |a Cellular and regional maintenance of iron homeostasis in the brain: normal and diseased states -- Iron deposits in brain disorders -- Brain iron and schizophrenia -- Some reflections on iron dependent free radical damage in the central nervous system -- Iron regulation of dopaminergic transmission: relevance to movement disorders -- Dopaminergic cell death in Parkinson’s disease: a role of iron? -- Iron and neurotoxin intoxication: comparative in vitro and in vivo studies -- Intranigral iron infusion in rats: A progressive model for excess nigral iron levels in Parkinson’s disease? -- Iron storage and transport markers in Parkinson’s disease and MPTP-treated mice -- Pathogenesis of Parkinson’s disease: iron and mitochondrial DNA deletion -- Consequences of intrastriatally administrated FeC13 and 6-OHDA without and after transient cerebral oligemia on behaviour and navigation -- Cytokine induced synthesis of nitric oxide from L-arginine: a cytotoxic mechanism that targets intracellular iron -- Lazaroids: potent inhibitors of iron-dependent lipid peroxidation for neurodegenerative disorders -- The treatment of iron overload — psychiatric implications -- Iron therapy: Pros and Cons 
653 |a Neurosciences 
653 |a Neurology  
653 |a Neurosciences 
653 |a Animal physiology 
653 |a Animal Physiology 
653 |a Neurology 
653 |a Pharmacology 
653 |a Pharmacology/Toxicology 
700 1 |a Youdim, M.B.H.  |e [editor] 
041 0 7 |a eng  |2 ISO 639-2 
989 |b SBA  |a Springer Book Archives -2004 
490 0 |a Key Topics in Brain Research 
856 4 0 |u https://doi.org/10.1007/978-3-7091-9322-8?nosfx=y  |x Verlag  |3 Volltext 
082 0 |a 616.8 
520 |a 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