Journal ArticleDOI
Inflammation and Alzheimer's disease.
Haruhiko Akiyama,Steven W. Barger,Scott R. Barnum,B Bradt,Jürgen Bauer,Greg M. Cole,Neil R. Cooper,Piet Eikelenboom,Mark R. Emmerling,Bernd L. Fiebich,Caleb E. Finch,Sally A. Frautschy,W. S. T. Griffin,Harald Hampel,Michael Hüll,Gary E. Landreth,Lih-Fen Lue,Robert E. Mrak,Ian R. A. Mackenzie,Patrick L. McGeer,M K O'Banion,Joel S. Pachter,Giulio Maria Pasinetti,C Plata-Salaman,Joseph G. Rogers,Russell E. Rydel,Yueyang Shen,Wolfgang J. Streit,Ronald Strohmeyer,I Tooyoma,F L van Muiswinkel,R. Veerhuis,David G. Walker,Scott D. Webster,Beatrice Hauss–Wegrzyniak,Gary L. Wenk,Tony Wyss-Coray +36 more
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.read more
Citations
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Journal ArticleDOI
Thrombin-Induced Oxidative Stress Contributes to the Death of Hippocampal Neurons In Vivo: Role of Microglial NADPH Oxidase
TL;DR: Thrombin-induced neurotoxicity in the hippocampus in vivo is caused by microglial NADPH oxidase-mediated oxidative stress, and suggests that thrombin inhibition or enhancing antioxidants may be beneficial for the treatment of neurodegenerative diseases, such as Alzheimer's disease, that are associated with microglia-derived oxidative damage.
Journal ArticleDOI
Differences of peripheral inflammatory markers between mild cognitive impairment and Alzheimer's disease
Paloma Bermejo,Sagrario Martín-Aragón,Juana Benedí,Cristina Susín,Emanuela Felici,Pedro Gil,José Manuel Ribera,Angel Villar +7 more
TL;DR: In conclusion, inflammatory response may be an early factor in AD development and these changes in circulating markers are possibly related to the progression of MCI to AD.
Journal ArticleDOI
Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties.
TL;DR: This study shows that EGCG prevents memory impairment as well as amyloidogenesis via inhibition of neuroinflammatory-related cytokines released from astrocytes and suggests that E GCG might be a useful intervention for neuroinflammation-associated AD.
Journal ArticleDOI
Tannic Acid is a Natural β-secretase Inhibitor that Prevents Cognitive Impairment and Mitigates Alzheimer-like Pathology in Transgenic Mice
Takashi Mori,Kavon Rezai-Zadeh,Naoki Koyama,Gary W. Arendash,Haruyasu Yamaguchi,Nobuto Kakuda,Yuko Horikoshi-Sakuraba,Jun Tan,Terrence Town,Terrence Town +9 more
TL;DR: The possibility that dietary supplementation with TA may be prophylactic for AD by inhibiting β-secretase activity and neuroinflammation and thereby mitigating AD pathology is raised.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
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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
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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)
Jürgen M. Lehmann,Linda B. Moore,Tracey Smith-Oliver,William O. Wilkison,Timothy M. Willson,Steven A. Kliewer +5 more
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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