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
Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease
Laura Gasparini,Marco Racchi,Giuliano Binetti,Marco Trabucchi,Sebastiano Bruno Solerte,Daniel L. Alkon,Rene Etcheberrigaray,Gary E. Gibson,John P. Blass,Rodolfo Paoletti,Stefano Govoni,Stefano Govoni +11 more
TL;DR: The use of peripheral tissues, particularly of cultured skin fibroblasts derived from AD patients, could complement studies of autopsy samples and provide a useful tool with which to investigate such dynamic processes as signal transduction systems, ionic homeostasis, oxidative metabolism, and APP processing.
Journal ArticleDOI
Invasion of hematopoietic cells into the brain of amyloid precursor protein transgenic mice.
Anna K. Stalder,Florian Ermini,Luca Bondolfi,Werner Krenger,Guido J. Burbach,Thomas Deller,Janaky Coomaraswamy,Matthias Staufenbiel,Regine Landmann,Mathias Jucker +9 more
TL;DR: Immunological and ultrastructural phenotyping revealed that macrophages and T-cells accounted for a significant portion of these ameboid-like invading cells, suggesting that hematopoietic cells invade the brain in response to cerebral amyloidosis may hold an unrecognized therapeutic potential.
Journal ArticleDOI
Does Alzheimer's disease begin in the brainstem?
Goran Šimić,Gabrijela Stanić,Mihovil Mladinov,Nataša Jovanov-Milošević,Ivica Kostović,Patrick R. Hof +5 more
TL;DR: In this article, a novel pathogenetic scheme of Alzheimer's disease progression was proposed based on these findings of differential susceptibility and anatomical connectivity, and the authors speculated that cumulative oxidative damage may be the main cause of DRN alterations, as the age is the main risk factor for sporadic AD.
Journal ArticleDOI
Th17 Cell-Mediated Neuroinflammation Is Involved in Neurodegeneration of Aβ1-42-Induced Alzheimer’s Disease Model Rats
TL;DR: Th17 cells, a subpopulation of CD4+ T cells with high proinflammation, participate in neuroinflammation and neurodegeneration of AD by release of proinflammatory cytokines and by direct action on neurons via Fas/FasL apoptotic pathway.
Journal ArticleDOI
Seizures and Epilepsy in Alzheimer's Disease
TL;DR: It is concluded that the literature on seizures and epilepsy in AD, including diagnosis, risk factors, and response to treatment suffers from methodological limitations and gaps.
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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