The role of netals in neurodegenerative processes: aluminum, manganese, and zinc. (Articolo in rivista)

Type
Label
  • The role of netals in neurodegenerative processes: aluminum, manganese, and zinc. (Articolo in rivista) (literal)
Anno
  • 2003-01-01T00:00:00+01:00 (literal)
Alternative label
  • Zatta P., Lucchini R., Van Rensburg S., Taylor A. (2003)
    The role of netals in neurodegenerative processes: aluminum, manganese, and zinc.
    in Brain research bulletin
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Zatta P., Lucchini R., Van Rensburg S., Taylor A. (literal)
Pagina inizio
  • 15 (literal)
Pagina fine
  • 28 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 62 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Titolo
  • The role of netals in neurodegenerative processes: aluminum, manganese, and zinc. (literal)
Abstract
  • Until last decade, little attention has been given by the neuroscience community to the neurometabolism. However, the neurobiology of heavy metals is now receiving interest, since it has been linked to the major neurodegenerative diseases. In the present review some metal that could possibly be involved in neurodegeneration are discussed. Two of them, manganese and zinc, are essential metals while aluminum is non-essential. Aluminum has long been known as a neurotoxic agent. It is an ethiopathogenic factor in diseases related to long-term dialysis treatment, and it has been controversially invoked as an aggravating factor or cofactor in Alzheimer¬ís disease as well as in other neurodegenerative diseases. Manganese exposure can play an important role in causing Parkinsonian disturbances, possibly enhancing physiological aging of the brain in comjunction with genetic predisposition. An increased environmental burden of manganese may have deleterious effects on more sensitive subgroups of the polupaltion, with sub.threshold neurodegeneration in the basal ganglia, generating a pre-Parkinsonian condition. In the case of zinc, there has as yet been no evidence that is involved in the etiology of neurodegenerative diseases in humans. Zinc is a redox-inactive and, as a result of efficient homeostasis control, does not accumulate in excess. However, adverse symptoms in human are abserved on inhalation of zinc fumes, or accidental injestion of unusually large amount of zinc. Also high concentrations of zinc have been found to kill bacteria, viruses, and cultured cells. Some of the possible mechanisms for cell death are reviewed. (literal)
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