Journal ArticleDOI
Inflammatory processes in Alzheimer's disease.
TLDR
While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle.About:
This article is published in Journal of Neuroimmunology.The article was published on 2007-03-01. It has received 895 citations till now. The article focuses on the topics: Gamma secretase & Amyloid beta.read more
Citations
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NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice
Michael T. Heneka,Markus P. Kummer,Andrea Stutz,Andrea Delekate,Stephanie Schwartz,Ana Vieira-Saecker,Angelika Griep,Daisy Axt,Anita Remus,Te-Chen Tzeng,Ellen Gelpi,Annett Halle,Martin Korte,Eicke Latz,Eicke Latz,Douglas T. Golenbock +15 more
TL;DR: The role of the NLRP3/caspase-1 axis in the pathogenesis of Alzheimer's disease was investigated in this article, which showed an important role for the inflammasome.
Journal ArticleDOI
Microglial physiology: unique stimuli, specialized responses
TL;DR: A wealth of data now demonstrate that the microglia have very diverse effector functions, in line with macrophage populations in other organs, and the term activatedmicroglia needs to be qualified to reflect the distinct and very different states of activation-associated effector function in different disease states.
Journal ArticleDOI
CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer
Cameron R. Stewart,Lynda M. Stuart,Kim Wilkinson,Janine M. van Gils,Jiusheng Deng,Annett Halle,Annett Halle,Katey J. Rayner,Laurent Boyer,Ruiqin Zhong,William A. Frazier,Adam Lacy-Hulbert,Joseph El Khoury,Douglas T. Golenbock,Kathryn J. Moore,Kathryn J. Moore +15 more
TL;DR: It is shown that oxidized LDL and amyloid-β trigger inflammatory signaling through a heterodimer of Toll-like receptors 4 and 6 that is regulated by signals from the scavenger receptor CD36, a common receptor for these disparate ligands.
Journal ArticleDOI
Clusters of hyperactive neurons near amyloid plaques in a mouse model of Alzheimer's disease.
Marc Aurel Busche,Gerhard Eichhoff,Gerhard Eichhoff,Helmuth Adelsberger,Helmuth Adelsberger,Dorothee Abramowski,Karl-Heinz Wiederhold,Christian Haass,Christian Haass,Matthias Staufenbiel,Arthur Konnerth,Arthur Konnerth,Olga Garaschuk,Olga Garaschuk +13 more
TL;DR: It is suggested that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides a mechanism for the disturbed cortical function in Alzheimer's disease.
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A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease.
Walter J. Lukiw,Jian Guo Cui,Victor L. Marcheselli,Merete Bodker,Anja Botkjaer,Katherine H. Gotlinger,Charles N. Serhan,Nicolas G. Bazan +7 more
TL;DR: Results indicate that NPD1 promotes brain cell survival via the induction of antiapoptotic and neuroprotective gene-expression programs that suppress Abeta42-induced neurotoxicity.
References
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Journal ArticleDOI
Microglia: a sensor for pathological events in the CNS
TL;DR: An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
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
TL;DR: 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.
Journal ArticleDOI
Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.
Dominic M. Walsh,Igor Klyubin,Julia V. Fadeeva,William K. Cullen,Roger Anwyl,Michael S. Wolfe,Michael J. Rowan,Dennis J. Selkoe +7 more
TL;DR: It is reported that natural oligomers of human Aβ are formed soon after generation of the peptide within specific intracellular vesicles and are subsequently secreted from the cell, indicating that synaptotoxic Aβ oligomers can be targeted therapeutically.
Journal ArticleDOI
Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction
Salvatore Oddo,Antonella Caccamo,Jason D. Shepherd,M. Paul Murphy,Todd E. Golde,Rakez Kayed,Raju Metherate,Mark P. Mattson,Yama Akbari,Frank M. LaFerla +9 more
TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.
Journal ArticleDOI
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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Inflammation and Alzheimer's disease.
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