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
Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease.
Maria I. Fonseca,Rahasson R. Ager,Shu Hui Chu,Ozkan Yazan,Sam D. Sanderson,Frank M. LaFerla,Stephen M. Taylor,Trent M. Woodruff,Andrea J. Tenner +8 more
TL;DR: Oral delivery of a cyclic hexapeptide C5a receptor antagonist for 2–3 mo resulted in substantial reduction of pathological markers such as fibrillar amyloid deposits and activated glia in two mouse models of AD, suggesting a novel therapeutic target for reducing pathology and improving cognitive function in human AD patients.
Journal ArticleDOI
Microglial chemotaxis, activation, and phagocytosis of amyloid β-peptide as linked phenomena in Alzheimer's disease
Joseph Rogers,Lih-Fen Lue +1 more
TL;DR: This work has shown that microglial chemotaxis, phagocytosis, and secretory activity in AD are necessarily coupled to localized inflammatory mechanisms that can be cytotoxic to nearby tissue.
Journal ArticleDOI
Antioxidants as treatment for neurodegenerative disorders
Bernd Moosmann,Christian Behl +1 more
TL;DR: The major challenges for drug development are the slow kinetics of disease progression, the unsolved mechanistic questions concerning the final causalities of cell death, the necessity to attain an effective permeation of the blood–brain barrier and the need to reduce the high concentrations currently required to evoke protective effects in cellular and animal model systems.
Journal ArticleDOI
How Do Immune Cells Support and Shape the Brain in Health, Disease, and Aging?
TL;DR: It is now understood that the barriers of the brain are not uniform in their interactions with the circulating immune cells, and Innate and adaptive immune cells are now known to have protective/healing properties in the CNS.
Journal ArticleDOI
Norepinephrine: The redheaded stepchild of Parkinson's disease.
TL;DR: The evidence that norepinephrine (NE) is neuroprotective and that LC degeneration sensitizes DA neurons to damage is examined, and the potential contribution of NE loss to the behavioral symptoms associated with PD is examined.
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
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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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