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dc.creatorMOREIRA,PAULA I
dc.creatorZHU,XIONGWEI
dc.creatorLIU,QUAN
dc.creatorHONDA,KAZUHIRO
dc.creatorSIEDLAK,SANDRA L
dc.creatorHARRIS,PEGGY L
dc.creatorSMITH,MARK A.
dc.creatorPERRY,GEORGE
dc.date2006-01-01
dc.date.accessioned2019-05-02T21:21:28Z
dc.date.available2019-05-02T21:21:28Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100002
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/81614
dc.descriptionOxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. In the first stage of development of the disease, amyloid-β deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. These findings suggest that Alzheimer disease is associated with a novel balance in oxidant homeostasis.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602006000100002
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.39 n.1 2006
dc.subjectAlzheimer disease
dc.subjectantioxidant therapy
dc.subjectmitochondria
dc.subjectoxidative stress
dc.subjectredox metals
dc.titleCompensatory responses induced by oxidative stress in Alzheimer disease


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