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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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Secretory PLA2-IIA: a new inflammatory factor for Alzheimer's disease

TL;DR: It is shown that sPLA2-IIA mRNA is up-regulated in Alzheimer's disease (AD) brains as compared to non-demented elderly brains (ND), and a higher percentage of sPLA 2-I IA-immunoreactive astrocytes present in AD hippocampus and inferior temporal gyrus.
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Multi-Target Directed Drugs: A Modern Approach for Design of New Drugs for the treatment of Alzheimer's Disease.

TL;DR: This review aims to show some recent advances and examples of the exploitation of MTDL approach in the rational design of novel drug candidate prototypes for the treatment of AD.
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Aspirin-Triggered Lipoxin A4 Stimulates Alternative Activation of Microglia and Reduces Alzheimer Disease–Like Pathology in Mice

TL;DR: It is demonstrated that aspirin-triggered LXA4 (15 μg/kg) s.c., twice a day, reduced NF-κB activation and levels of proinflammatory cytokines and chemokines, as well as increased levels of anti-inflammatory IL-10 and transforming growth factor-β, leading to improved phagocytic function, promoting clearance of Aβ deposits and ultimately leading to reduction in synaptotoxicity and improvement in cognition.
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Lycopene abrogates Aβ(1-42)-mediated neuroinflammatory cascade in an experimental model of Alzheimer's disease.

TL;DR: The amelioration of Aβ1-42-induced spatial learning and memory impairment by lycopene could be linked, at least in part, to the inhibition of NF-κB activity and the down-regulation of expression of neuroinflammatory cytokines, suggesting that lycopenes may be a potential candidate for AD treatment.
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Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration

TL;DR: Evidence is presented demonstrating that fibrin deposition increases in the AD brain and correlates with the degree of pathology and support the design of therapeutic strategies aimed at blocking the interaction betweenfibrinogen and amyloid-β (Aβ) and/or normalizing the increased thrombosis present in AD.
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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