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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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Cognitive-enhancing activity of thymol and carvacrol in two rat models of dementia.

TL;DR: Positive evidence is provided for the effectiveness and safety of thymol and carvacrol in alleviating cognitive impairments caused by increased A&bgr; levels or cholinergic hypofunction and Anticholinesterase, antioxidant, and anti-inflammatory activities may be the mechanisms contributing toward their beneficial effects in these models.
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Beta-amyloid protein structure determines the nature of cytokine release from rat microglia.

TL;DR: The responses of microglia to different forms of Aβ, with regard to release of the proinflammatory cytokines interleukin-1α, IL-1β, tumor necrosis factor-α, TNF-α), IL-6, and interferon-γ (IFN-γ) were analyzed.
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Association between Periodontitis and Alzheimer's Disease.

TL;DR: The present review throws a light on possible enigmatic link between AD and periodontitis by collecting data from PubMed database using key words like "Alzheimer′s disease", "inflammation", "periodontitis", and "proinflammatory cytokines".
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Loss of perineuronal net N-acetylgalactosamine in Alzheimer’s disease

TL;DR: In AD, there is marked loss of PN GalNAc that is not topographically related to neurofibrillary pathology, parenchymal Aβ load or activated microglia, which is likely to impair the function of these inhibitory interneurons.
Journal ArticleDOI

Innate Immunity Fights Alzheimer's Disease

TL;DR: It is hypothesize that rebalancing cerebral innate immunity by inhibiting actions of key anti-inflammatory cytokines returns the brain to a physiological state and represents an important step toward innate immune-targeted therapy to combat AD.
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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