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
Neuroinflammation, COX-2, and ALS—a dual role?
TL;DR: The pathways of COX activity and prostaglandin production form the center of the debate regarding the dual nature of neuroinflammation and how this duality may affect future treatments for neurodegenerative diseases such as ALS is discussed.
Journal ArticleDOI
Beta amyloid peptide (Abeta42) is internalized via the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in macrophages.
Hiroshi Yazawa,Zu-Xi Yu,Takeda,Yingying Le,Wanghua Gong,Victor J. Ferrans,Joost J. Oppenheim,Chou Chi H. Li,Ji Ming Wang +8 more
TL;DR: The results suggest that besides mediating the proinflammatory activity of Aβ42, FPRL1 is also involved in the internalization of A β42, which culminates in the formation of fibrils only in macrophages.
Journal ArticleDOI
Neuroinflammation, microglia and implications for anti-inflammatory treatment in Alzheimer's disease.
Daniela Krause,Norbert Müller +1 more
TL;DR: Light is shed on whether neuroinflammation is associated to brain tissue damage and functional impairment or is there also a damage limiting activity and the limitations and the advantages of anti-inflammatory treatment options.
Journal ArticleDOI
Microglial activation in Alzheimer's disease: an (R)-[¹¹C]PK11195 positron emission tomography study
Alie Schuitemaker,Marc A Kropholler,Ronald Boellaard,Wiesje M. van der Flier,Reina W. Kloet,Thalia F. van der Doef,Thalia F. van der Doef,Dirk L. Knol,Albert D. Windhorst,Gert Luurtsema,Frederik Barkhof,Cees Jonker,Adriaan A. Lammertsma,Philip Scheltens,Bart N.M. van Berckel +14 more
TL;DR: Microglial activation is a subtle phenomenon occurring in AD, and BP(ND) did not correlate with cognitive function.
Journal ArticleDOI
Porphyromonas gingivalis Periodontal Infection and Its Putative Links with Alzheimer's Disease.
TL;DR: The aim of this review is to discuss the relevance of finding the keystone periodontal pathogen P. gingivalis in AD brains and its plausible contribution to the aetiological hypothesis of this dementing condition.
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
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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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