Early Onset Alzheimer's Disease and Oxidative Stress

被引:47
作者
Antonio Meraz-Rios, Marco [1 ]
Franco-Bocanegra, Diana [2 ]
Toral Rios, Danira [3 ]
Campos-Pena, Victoria [4 ]
机构
[1] Inst Politecn Nacl, Dept Biomed Mol, Ctr Invest & Estudios Avanzados, Mexico City 07360, DF, Mexico
[2] Univ Nacl Autonoma Mexico, Mexico City 04510, DF, Mexico
[3] Inst Politecn Nacl, Dept Fisiol Biofis & Neurociencias, Ctr Invest & Estudios Avanzados, Mexico City 07360, DF, Mexico
[4] Inst Nacl Neurol & Neurocirugia Manuel Velasco Su, Lab Expt Enfermedades Neurodegenerat, Mexico City 14269, DF, Mexico
关键词
AMYLOID PRECURSOR PROTEIN; GAMMA-SECRETASE ACTIVITY; PAIRED HELICAL FILAMENT; A-BETA; APOLIPOPROTEIN-E; IN-VITRO; PRESENILIN; TAU-PROTEIN; NEURODEGENERATIVE DISEASES; MITOCHONDRIAL DYSFUNCTION;
D O I
10.1155/2014/375968
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Alzheimer's disease (AD) is the most common cause of dementia in elderly adults. It is estimated that 10% of the world's population aged more than 60-65 years could currently be affected by AD, and that in the next 20 years, there could be more than 30 million people affected by this pathology. One of the great challenges in this regard is that AD is not just a scientific problem; it is associated with major psychosocial and ethical dilemmas and has a negative impact on national economies. The neurodegenerative process that occurs in AD involves a specific nervous cell dysfunction, which leads to neuronal death. Mutations in APP, PS1, and PS2 genes are causes for early onset AD. Several animal models have demonstrated that alterations in these proteins are able to induce oxidative damage, which in turn favors the development of AD. This paper provides a review of many, although not all, of the mutations present in patients with familial Alzheimer's disease and the association between some of these mutations with both oxidative damage and the development of the pathology.
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页数:14
相关论文
共 154 条
[1]
β-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase [J].
Abramov, AY ;
Canevari, L ;
Duchen, MR .
JOURNAL OF NEUROSCIENCE, 2004, 24 (02) :565-575
[2]
Interaction of nascent ApoE2, ApoE3, and ApoE4 isoforms expressed in mammalian cells with amyloid peptide beta (1-40). Relevance to Alzheimer's disease [J].
Aleshkov, S ;
Abraham, CR ;
Zannis, VI .
BIOCHEMISTRY, 1997, 36 (34) :10571-10580
[3]
Unusual phenotypic alteration of β amyloid precursor protein (βAPP) maturation by a new Val-715→Met βAPP-770 mutation responsible for probable early-onset Alzheimer's disease [J].
Ancolio, K ;
Dumanchin, C ;
Barelli, H ;
Warter, JM ;
Brice, A ;
Campion, D ;
Frébourg, T ;
Checler, F .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (07) :4119-4124
[4]
STRUCTURE AND NOVEL EXONS OF THE HUMAN-TAU GENE [J].
ANDREADIS, A ;
BROWN, WM ;
KOSIK, KS .
BIOCHEMISTRY, 1992, 31 (43) :10626-10633
[5]
Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-amyloid plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology [J].
Apelt, J ;
Bigl, M ;
Wunderlich, P ;
Schliebs, R .
INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE, 2004, 22 (07) :475-484
[6]
Tau-mediated neurodegeneration in Alzheimer's disease and related disorders [J].
Ballatore, Carlo ;
Lee, Virginia M. -Y. ;
Trojanowski, John Q. .
NATURE REVIEWS NEUROSCIENCE, 2007, 8 (09) :663-672
[7]
Neurotoxic, redox-competent Alzheimer's β-amyloid is released from lipid membrane by methionine oxidation [J].
Barnham, KJ ;
Ciccotosto, GD ;
Tickler, AK ;
Ali, FE ;
Smith, DG ;
Williamson, NA ;
Lam, YH ;
Carrington, D ;
Tew, D ;
Kocak, G ;
Volitakis, I ;
Separovic, F ;
Barrow, CJ ;
Wade, JD ;
Masters, CL ;
Cherny, RA ;
Curtain, CC ;
Bush, AI ;
Cappai, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (44) :42959-42965
[8]
Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice [J].
Begley, JG ;
Duan, WZ ;
Chan, S ;
Duff, K ;
Mattson, MP .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (03) :1030-1039
[9]
The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes [J].
Benilova, Iryna ;
Karran, Eric ;
De Strooper, Bart .
NATURE NEUROSCIENCE, 2012, 15 (03) :349-357
[10]
Presenilin clinical mutations can affect γ-secretase activity by different mechanisms [J].
Bentahir, M ;
Nyabi, O ;
Verhamme, J ;
Tolia, A ;
Horré, K ;
Wiltfang, J ;
Esselmann, H ;
De Strooper, B .
JOURNAL OF NEUROCHEMISTRY, 2006, 96 (03) :732-742