Proposing biomarkers to evaluate the alterations in the brain iron homeostasis and their relation with the physiopathology of Alzheimer's disease Proponiendo biomarcadores para evaluar las alteraciones en la homeostasis cerebral de hierro y su relación co
Author
dc.contributor.author
Tapia-Saavedra, Alexis
Admission date
dc.date.accessioned
2019-03-11T12:54:01Z
Available date
dc.date.available
2019-03-11T12:54:01Z
Publication date
dc.date.issued
2007
Cita de ítem
dc.identifier.citation
Revista Chilena de Neuro-Psiquiatria, Volumen 45, Issue 1, 2018, Pages 29-41
Identifier
dc.identifier.issn
00347388
Identifier
dc.identifier.issn
07179227
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/164316
Abstract
dc.description.abstract
Multiple lines of evidence have implicated oxidative stress and free radical damage to the pathogenesis and etiology of Alzheimer's disease (AD). Amyloid-beta peptide contributes to oxidative damage in AD by inducing lipid peroxidation. In addition, iron might contribute to the increased susceptibility of the brain to iron-induced oxidative damage, due to its ability to catalyze the generation of free radicals in biological systems. There are several points in the iron regulation pathway in which alterations may occur, affecting iron metabolism. Altered expression and altered cellular distribution of melanotransferrin, lactotransferrin, and neuromelanin have been reported in the brain tissue of patients suffering AD. In addition, disruptions in lactotransferrin, ceruloplasmin, neuromelanin, and hemo oxygenase may result in oxidative stress. In conclusion, in AD it appears to be an excessive accumulation of iron in the brain and oxidative damage, suggesting a loss of the homeostatic mec
Proposing biomarkers to evaluate the alterations in the brain iron homeostasis and their relation with the physiopathology of Alzheimer's disease Proponiendo biomarcadores para evaluar las alteraciones en la homeostasis cerebral de hierro y su relación co