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
Insulin in the brain: its pathophysiological implications for States related with central insulin resistance, type 2 diabetes and Alzheimer's disease.
Enrique Blázquez,Enrique Blázquez,Esther Velázquez,Esther Velázquez,Verónica Hurtado-Carneiro,Verónica Hurtado-Carneiro,Juan Miguel Ruiz-Albusac,Juan Miguel Ruiz-Albusac +7 more
TL;DR: Advances in the knowledge of preclinical AD and T2DM may be a major stimulus for the development of treatment for preventing the pathogenic events of these disorders, mainly those focused on reducing brain insulin resistance, which is seems to be a common ground for both pathological entities.
Journal ArticleDOI
Neuroprotective and disease-modifying effects of the ketogenic diet
TL;DR: There is evidence that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke.
Journal ArticleDOI
Neuroinflammation in Alzheimer's disease and prion disease.
Piet Eikelenboom,Clive Bate,W.A. van Gool,Jeroen J.M. Hoozemans,J. M. Rozemuller,R. Veerhuis,A. Williams +6 more
TL;DR: In this article, the similarities and differences between the involvement of inflammatory mechanisms in Alzheimer's disease and prion disease are discussed. And the concept that the demonstration of a chronic inflammatory-like process relatively early in the pathological cascade of both diseases suggests potential therapeutic strategies to prevent or to retard these chronic neurodegenerative disorders.
Journal ArticleDOI
How does diabetes accelerate Alzheimer disease pathology
TL;DR: A summary of the mechanistic pathways that might link diabetes and AD is summarized, necessary for the development of novel drug therapies and lifestyle guidelines aimed at the treatment and/or prevention of these diseases.
Journal ArticleDOI
Occurrence of T cells in the brain of Alzheimer's disease and other neurological diseases.
Takashi Togo,Haruhiko Akiyama,Eizo Iseki,Hiromi Kondo,Kenji Ikeda,Masanori Kato,Tatsuro Oda,Kuniaki Tsuchiya,Kenji Kosaka +8 more
TL;DR: The phenotype of T cells in the AD brain indicates that they are activated but are not fully differentiated, and local inflammatory conditions might cause accumulation and activation of T cell in theAD brain.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
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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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