Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/7876
DC FieldValueLanguage
dc.contributor.authorCastellani, Rudy-
dc.contributor.authorMoreira, Paula-
dc.contributor.authorLiu, Gang-
dc.contributor.authorDobson, Jon-
dc.contributor.authorPerry, George-
dc.contributor.authorSmith, Mark-
dc.contributor.authorZhu, Xiongwei-
dc.date.accessioned2009-02-17T10:36:30Z-
dc.date.available2009-02-17T10:36:30Z-
dc.date.issued2007en_US
dc.identifier.citationNeurochemical Research. 32:10 (2007) 1640-1645en_US
dc.identifier.urihttps://hdl.handle.net/10316/7876-
dc.description.abstractAbstract Although iron is essential in maintaining the function of the central nervous system, it is a potent source of reactive oxygen species. Excessive iron accumulation occurs in many neurodegenerative diseases including Alzheimer disease (AD), Parkinson’s disease, and Creutzfeldt-Jakob disease, raising the possibility that oxidative stress is intimately involved in the neurodegenerative process. AD in particular is associated with accumulation of numerous markers of oxidative stress; moreover, oxidative stress has been shown to precede hallmark neuropathological lesions early in the disease process, and such lesions, once present, further accumulate iron, among other markers of oxidative stress. In this review, we discuss the role of iron in the progression of AD.en_US
dc.language.isoengeng
dc.publisherSpringer Netherlands-
dc.rightsopenAccesseng
dc.titleIron: The Redox-active Center of Oxidative Stress in Alzheimer Diseaseen_US
dc.typearticleen_US
dc.identifier.doi10.1007/s11064-007-9360-7en_US
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypearticle-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.fulltextCom Texto completo-
item.languageiso639-1en-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0001-5177-6747-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
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