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P3–371: Mitochondrial GSH depletion sensitizes human neuroblastoma cells to beta–amyloid peptide–induced oxidative stress and apoptotic cell death
Author(s) -
Colell Anna,
Fernandez Anna,
Fernandez-Checa Jose C.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.1641
Subject(s) - mitochondrion , oxidative stress , reactive oxygen species , lipid peroxidation , microbiology and biotechnology , glutathione , programmed cell death , apoptosis , amyloid beta , cytosol , biology , chemistry , biochemistry , peptide , enzyme
Comunicación 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)The 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.Peer Reviewe