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Mitochondrial GSH depletion sensitizes human neuroblastoma cells to beta-amyloid peptide-induced oxidative stress and apoptotic cell death

AuthorsColell Riera, Anna ; Fernández, Anna; Fernández-Checa, José C.
Issue Date1-Jul-2006
PublisherAlzheimer’s Association
CitationAlzheimer's and Dementia 2(3, supplement): S484-S485 (2006)
AbstractThe pathogenesis of Alzheimer disease is not completely understood at present, although the generation of toxic beta-amyloid peptide (Aβ) is thought to play a prominent role. One of the cytotoxic effects of the Aβ is reactive oxygen species (ROS) overgeneration. Although, the exact mechanisms of this process are not well defined, emerging evidence points to mitochondria as a source for Aβ-induced ROS generation. Moreover, disturbances in cholesterol homeostasis promote the formation and deposition of Aβ and the progression of AD.
DescriptionComunicación presentada en la Alzheimer's Association 10th International Conference on Alzheimer's Disease and Related Disorders, celebrada del 15 al 20 de julio de 2006 en Madrid (España)
Publisher version (URL)http://dx.doi.org/10.1016/j.jalz.2006.05.1641
Identifiersdoi: 10.1016/j.jalz.2006.05.1641
issn: 1552-5260
Appears in Collections:(IIBB) Comunicaciones congresos
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