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- W1542830050 abstract "The aging process is believed to be closely related to increased oxidative stress. Reactive intermediates of oxidative stress affect the cellular redox status and induce apoptosis [1]. Oxidative stress due to the loss of balance between ROS production and antioxidant defenses affects all the vital organs, resulting in aging [1,2]. Oxidative damage, mitochondrial dysfunc‐ tion and inflammation underlies many common aging-related neurodegenerative diseases, including AD [2,3]. The major pathological hallmark of AD is the accumulation of Aβ peptides in the brain [4]. Oxidative insults that induce neuronal apoptosis, including agents that induce membrane lipid peroxidation, also have been shown to activate caspases [5]. Increased lipid peroxidation was consistently observed in some animal models of Alzheimer amyloidosis [4, 6]. It has been shown that a single Aβ administration into the rat hippocampus could induce increase of NOS activity and NO level [6]. Nitric oxide is a multifunctional molecule that acts as messenger/modulator in synaptogenesis and potential neurotoxin and is synthesized by three isozymes of Nitric oxide synthase (NOS) [7]. Oxidative stress reflects a situation in which ROS is continuously produced and exceeds the capacity of endogenous antioxidant defense systems. Several studies have suggested that oxidative stress plays a key role in Aβ-mediated neuronal cytotoxicity by triggering or facilitating neurodegeneration through a wide range of molecular events that eventually lead to neuronal cell loss. Aβ significantly increases produc‐ tion and enhances membrane lipid peroxidation, leading to neuronal apoptosis [8,9]. Because multiple factors are involved in the pathogenesis of the AD, it is difficult to find an ideal in vivo model. It is important to determine Aβ 1-42 injection effects especially in hippocampus," @default.
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- W1542830050 date "2013-05-15" @default.
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- W1542830050 title "Role of Oxidative Stress in Aβ Animal Model of Alzheimer's Disease: Vicious Circle of Apoptosis, Nitric Oxide and Age" @default.
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- W1542830050 doi "https://doi.org/10.5772/54718" @default.
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