Abstract
Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. The review summarizes the facts about redox-signaling cascade in the cells operating through an array of kinases, phosphatases and transcription factors and their downstream components. The biology of NF-κB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. The possibility of identifying new disease-modifying drugs for AD targeting NF-κBsignaling cascade has been discussed in the end.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / metabolism
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / antagonists & inhibitors*
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Amyloid beta-Peptides / metabolism
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Animals
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Antioxidants / chemical synthesis*
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Antioxidants / therapeutic use
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Brain / drug effects
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Brain / metabolism
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Brain / pathology
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Curcumin / pharmacology
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Cytokines / antagonists & inhibitors
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Cytokines / genetics
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Cytokines / metabolism
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Diterpenes, Kaurane / pharmacology
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Gene Expression Regulation
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Humans
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Mice
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NF-kappa B / antagonists & inhibitors*
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NF-kappa B / genetics
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NF-kappa B / metabolism
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Neuroprotective Agents / chemical synthesis*
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Neuroprotective Agents / therapeutic use
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Oxidative Stress / drug effects
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Reactive Oxygen Species / antagonists & inhibitors
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Reactive Oxygen Species / metabolism
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Signal Transduction / drug effects
Substances
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Amyloid beta-Peptides
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Antioxidants
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Cytokines
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Diterpenes, Kaurane
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NF-kappa B
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Neuroprotective Agents
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Reactive Oxygen Species
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oridonin
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Curcumin