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Journal ArticleDOI

Inflammation and Alzheimer's disease.

TLDR
By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
About
This article is published in Neurobiology of Aging.The article was published on 2000-05-01. It has received 4319 citations till now. The article focuses on the topics: Alzheimer's disease & Neuroinflammation.

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Citations
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A Meta-Analysis of Cytokines in Alzheimer's Disease

TL;DR: The results strengthen the clinical evidence that AD is accompanied by an inflammatory response, particularly higher peripheral concentrations of IL-6, TNF-α, IL-1β, TGF-β,IL-12 and IL-18 and higher CSF concentrations of T GF-β.
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Inflammation in Alzheimer Disease—A Brief Review of the Basic Science and Clinical Literature

TL;DR: Biochemical and neuropathological studies of brains from individuals with Alzheimer disease provide clear evidence for an activation of inflammatory pathways, and long-term use of anti-inflammatory drugs is linked with reduced risk to develop the disease.
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Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

TL;DR: The interrelationships between Neuroinflammation and amyloid and tau pathologies as well as the effect of neuroinflammation on the disease trajectory in AD are discussed, focusing on microglia as major players in neuro inflammation and how these cells could be modulated as a therapeutic strategy for AD.
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Inflammatory mediators in the elderly

TL;DR: It is possible that inflammatory mediators constitute a link between life style factors, infections and physiological changes in the process of ageing on the one hand and risk factors for age-associated diseases on the other.
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An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations

TL;DR: Mechanisms of in vivo ROS generation are described, the potential impact of ROS and oxidative damage on cellular function is examined, and how these responses change with aging in physiologically relevant situations are evaluated.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs

TL;DR: Experiments with guinea-pig lung suggest that some of the therapeutic effects of sodium salicylate and aspirin-like drugs are due to inhibition of the synthesis of prostaglandins.
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TGF-beta signal transduction.

TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
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An endotoxin-induced serum factor that causes necrosis of tumors

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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Chemokines — Chemotactic Cytokines That Mediate Inflammation

TL;DR: This review introduces the burgeoning family of cytokines, with special emphasis on their role in the pathophysiology of disease and their potential as targets for therapy.
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An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor γ (PPARγ)

TL;DR: It is reported that thiazolidinediones are potent and selective activators of peroxisome proliferator-activated receptor γ (PPARγ), a member of the nuclear receptor superfamily recently shown to function in adipogenesis, and raised the intriguing possibility that PPARγ is a target for the therapeutic actions of this class of compounds.
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