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
Chronic brain inflammation results in cell loss in the entorhinal cortex and impaired LTP in perforant path-granule cell synapses.
TL;DR: Chronic neuroinflammation produced by chronic infusion of lipopolysaccharide into the fourth ventricle for 4 weeks upon the induction and maintenance of long-term potentiation (LTP) in the dentate gyrus of the hippocampus, a well-characterized model of cellular synaptic plasticity results in the loss of pyramidal cells within layers II and III of the entorhinal cortex.
Journal ArticleDOI
Positron emission tomography imaging of neuroinflammation.
TL;DR: A profile of active disease emerges that matches some of the typical distribution patterns known from structural neuroimaging techniques, but additionally shows involvement of brain regions linked through neural pathways, in the context of cell-based in vivo neuropathology.
Journal ArticleDOI
Active invasion of Porphyromonas gingivalis and infection-induced complement activation in ApoE-/- mice brains.
Sophie Poole,Simarjit Kaur Singhrao,Sasanka S. Chukkapalli,Mercedes F. Rivera,Irina M. Velsko,Lakshmyya Kesavalu,St John Crean +6 more
TL;DR: Results show that the oral pathogen P. gingivalis was able to access the ApoE-/- mice brain and thereby contributed to complement activation with bystander neuronal injury.
Journal ArticleDOI
Evidence for systemic immune system alterations in sporadic amyotrophic lateral sclerosis (sALS)
Rongzhen Zhang,Ron Gascon,Robert G. Miller,Deborah F. Gelinas,Jason Mass,Ken Hadlock,Xia Jin,Jeremy Reis,Amy Narvaez,Michael S. McGrath +9 more
TL;DR: In this article, the degree of activation was directly related to the rate of sALS disease progression and other parameters of T-cell activation and immune globulin levels showed similar disease associated changes.
Journal ArticleDOI
Amyloid β-peptide1–42 alters tight junction protein distribution and expression in brain microvessel endothelial cells
Sonia Marco,Stephen D. Skaper +1 more
TL;DR: It is suggested that Aβ 1–42 effects on tight junction protein complexes may alter blood–brain barrier integrity and contribute to the neuropathological sequelae of Alzheimer's disease.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
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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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