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
Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer's disease.
TL;DR: The role of neuroinflammation in the chronicity of AD pathogenesis is described and an overview of the recent research towards the development of new therapies to treat this disorder is described.
Journal ArticleDOI
Induction of Tau Pathology by Intracerebral Infusion of Amyloid-β-Containing Brain Extract and by Amyloid-β Deposition in APP × Tau Transgenic Mice
Tristan Bolmont,Florence Clavaguera,Melanie Meyer-Luehmann,Martin C. Herzig,Rebecca Radde,Matthias Staufenbiel,Jada Lewis,Mike Hutton,Markus Tolnay,Mathias Jucker +9 more
TL;DR: It is suggested that both extract-derived Aβ species and deposited fibrillary Aβ can induce the formation of tau neurofibrillary pathology, and provides an explanation for the discrepancy between the neuroanatomical location of Aβ deposits and the development and spreading of t Tau lesions in Alzheimer's disease brain.
Journal ArticleDOI
Central effects of GLP-1: new opportunities for treatments of neurodegenerative diseases.
TL;DR: GLP-1 mimetics show great promise as a novel treatment for neurodegenerative conditions because of the substantial body of evidence that these mimetics have neuroprotective and anti-inflammatory effects.
Journal ArticleDOI
β-Amyloid-Stimulated Microglia Induce Neuron Death via Synergistic Stimulation of Tumor Necrosis Factor α and NMDA Receptors
TL;DR: The hypothesis that AD brains provide the appropriate microglial-mediated inflammatory environment for TNFα and glutamate to synergistically stimulate toxic activation of their respective signaling pathways in neurons as a contributing mechanism of cell death is suggested.
Journal ArticleDOI
Generation of Aggregated β-Amyloid in the Rat Hippocampus Impairs Synaptic Transmission and Plasticity and Causes Memory Deficits
TL;DR: It is suggested that aggregated amyloid material induces cognitive deficits similar to those observed in the early phases of Alzheimer's disease via an alteration in neuronal transmission and plasticity.
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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