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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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The role of cyclo-oxygenase 1 and 2 activity in prostaglandin E2 secretion by cultured human adult microglia: Implications for Alzheimer's disease

TL;DR: The data presented in this study suggest that classical NSAIDs, rather than selective COX-2 inhibitors, are more potent in reducing microglial prostaglandin secretion.
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Calorie restriction ameliorates neurodegenerative phenotypes in forebrain-specific presenilin-1 and presenilin-2 double knockout mice.

TL;DR: It is found that CR improved novel object recognition and contextual fear conditioning memory in the cDKO mice and could increase the expression of neurogenesis related genes and decrease theexpression of inflammation related genes in the hippocampus of cD KO mice.
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Role of TGFβ signaling in the pathogenesis of Alzheimer’s disease

TL;DR: It is discussed that changes of TGFβ-mediated regulation could at least partially mediate age-associated microglia changes, and, together with other changes on inflammatory response, could result in the reduction of protective activation and the potentiation of cytotoxicity ofmicroglia, resulting in the promotion of neurodegenerative diseases.
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Ibuprofen attenuates oxidative damage through NOX2 inhibition in Alzheimer's disease

TL;DR: It is suggested that ibuprofen acts independently of cyclooxygenase COX inhibition to disrupt signaling cascades leading to microglial NADPH oxidase (NOX2) activation, preventing oxidative damage and enhancing plaque clearance in the brain.
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Deficiency in BDNF/TrkB Neurotrophic Activity Stimulates δ-Secretase by Upregulating C/EBPβ in Alzheimer's Disease.

TL;DR: These findings provide a mechanistic link between BDNF/TrkB reduction, C/EBPβ upregulation, δ-secretase activity, and Aβ and Tau alterations in murine brains and rescue impaired synaptic plasticity and cognitive dysfunctions.
References
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Journal ArticleDOI

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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