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
Astrocytic A beta 1-42 uptake is determined by A beta-aggregation state and the presence of amyloid-associated proteins.
Henrietta M. Nielsen,Sandra D. Mulder,Jeroen A.M. Beliën,René J. P. Musters,Piet Eikelenboom,Robert Veerhuis +5 more
TL;DR: Astrocytic uptake of Aβfib increased when added to the cells in combination with SAP and C1q (SAP/C1q), but was unchanged in the presence of ApoE, ApoJ and ACT, which indicates that amyloid‐associated proteins, especially Apo J and Apo E, can alter Aβ‐uptake in vitro and hence may influence Aβ clearance and plaque formation in vivo.
Journal ArticleDOI
Neurovascular function in Alzheimer's disease patients and experimental models
Nektaria Nicolakakis,Edith Hamel +1 more
TL;DR: The following paper will present the elements of AD neurovascular dysfunction and review the in vitro and in vivo model systems that have served to deepen the understanding of it, and critically evaluate selected groups of compounds, the FDA-approved cholinesterase inhibitors and thiazolidinediones, for their ability to correct neurov vascular dysfunction in AD patients and models.
Journal ArticleDOI
Inflammation and NF-kappa B in Alzheimer's Disease and Diabetes
TL;DR: The authors reviewed the literature on how inflammation and the inducible nuclear factor NF-kappaB might be involved in both diabetes mellitus and Alzheimer's disease and whether these factors can link both diseases.
Journal ArticleDOI
Insulin and Alzheimer's disease: untangling the web.
TL;DR: A brief description of the role of insulin in normal brain function is provided, and more closely on recent evidence regarding the mechanisms through which disruption of that role may promote AD pathological processes are focused on.
Journal ArticleDOI
Vascular Remodeling versus Amyloid β-Induced Oxidative Stress in the Cerebrovascular Dysfunctions Associated with Alzheimer's Disease
TL;DR: It is concluded that brain vessel remodeling and associated alterations in levels of vasoactive signaling molecules are key contributors to AD cerebrovascular dysfunctions.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
TL;DR: Experiments with guinea-pig lung suggest that some of the therapeutic effects of sodium salicylate and aspirin-like drugs are due to inhibition of the synthesis of prostaglandins.
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TGF-beta signal transduction.
TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
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An endotoxin-induced serum factor that causes necrosis of tumors
TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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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.
Journal ArticleDOI
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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