Journal ArticleDOI
Oxidative stress, protein modification and Alzheimer disease.
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TLDR
Evidence demonstrating the oxidation/dysfunction of a number of enzymes specifically involved in energy metabolism that support the view that reduced glucose metabolism and loss of ATP are crucial events triggering neurodegeneration and progression of AD is discussed.About:
This article is published in Brain Research Bulletin.The article was published on 2017-07-01. It has received 218 citations till now. The article focuses on the topics: Neurodegeneration & Protein oxidation.read more
Citations
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Oxidative stress and the amyloid beta peptide in Alzheimer's disease.
Clémence Cheignon,M. Tomas,M. Tomas,Dominique Bonnefont-Rousselot,Peter Faller,Christelle Hureau,Christelle Hureau,Fabrice Collin,Fabrice Collin +8 more
TL;DR: This review highlights the existing link between oxidative stress and AD, and the consequences towards the Aβ peptide and surrounding molecules in terms of oxidative damage, along with the implication of metal ions in AD.
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Eric Tönnies,Eugenia Trushina +1 more
TL;DR: The role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease are discussed.
Journal ArticleDOI
Chemical Basis of Reactive Oxygen Species Reactivity and Involvement in Neurodegenerative Diseases
TL;DR: This review highlights the production and regulation of ROS, their chemical properties, both from kinetic and thermodynamic points of view, the links between them, and their implication in neurodegenerative diseases.
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Endogenous non-enzymatic antioxidants in the human body.
TL;DR: This paper focuses on the major intrinsic non-enzymatic antioxidants, including metal binding proteins (MBPs), glutathione (GSH), uric acid (UA), melatonin (MEL), bilirubin (BIL) and polyamines (PAs).
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Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease.
TL;DR: It is opine that targeting altered pathways secondary to oxidative damage in brain from persons with AD, aMCI, or Down syndrome with AD may provide strategies to slow or perhaps one day, prevent, progression or development of this devastating dementing disorder.
References
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Journal ArticleDOI
Alzheimer's Disease: Genes, Proteins, and Therapy
TL;DR: Evidence that the presenilin proteins, mutations in which cause the most aggressive form of inherited AD, lead to altered intramembranous cleavage of the beta-amyloid precursor protein by the protease called gamma-secretase has spurred progress toward novel therapeutics and provided discrete biochemical targets for drug screening and development.
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Current concepts in mild cognitive impairment.
Ronald C. Petersen,Rachelle S. Doody,Alexander Kurz,Richard C. Mohs,John C. Morris,Peter V. Rabins,Karen Ritchie,Martin N. Rossor,Leon J. Thal,Bengt Winblad +9 more
TL;DR: A group of experts on aging and MCI from around the world in the fields of neurology, psychiatry, geriatrics, neuropsychology, neuroimaging, neuropathology, clinical trials, and ethics was convened to summarize the current state of the field of MCI.
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Amyloid plaque core protein in Alzheimer disease and Down syndrome
Colin L. Masters,Gail Simms,Nicola A. Weinman,Gerd Multhaup,Brian L. McDonald,Konrad Beyreuther +5 more
TL;DR: The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.
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Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins
Mary P. Lambert,A. K. Barlow,Brett A. Chromy,C. Edwards,R. Freed,M. Liosatos,Todd E. Morgan,Irina Rozovsky,Barbara L. Trommer,Kirsten L. Viola,Pat Wals,Chuan Zhang,Caleb E. Finch,Grant A. Krafft,William L. Klein +14 more
TL;DR: It is hypothesized that impaired synaptic plasticity and associated memory dysfunction during early stage Alzheimer's disease and severe cellular degeneration and dementia during end stage could be caused by the biphasic impact of Abeta-derived diffusible ligands acting upon particular neural signal transduction pathways.
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Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling
TL;DR: This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival, ROS homeostasis and antioxidant gene regulation, mitochondrial oxidative stress, apoptosis, and aging.