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
Amyloid β Oligomers Disrupt Blood–CSF Barrier Integrity by Activating Matrix Metalloproteinases
Marjana Brkic,Sriram Balusu,Elien Van Wonterghem,Nina Gorlé,Iryna Benilova,Anna Kremer,Inge Van Hove,Lieve Moons,Bart De Strooper,Selma Kanazir,Claude Libert,Roosmarijn E. Vandenbroucke +11 more
TL;DR: The results reveal that Alzheimer's disease-associated soluble Aβ1–42 oligomers induce BCSFB dysfunction and suggest MMPs as a possible therapeutic target, and suggest that MMP inhibition might have therapeutic potential.
Journal ArticleDOI
NSAID and Antioxidant Prevention of Alzheimer's Disease: Lessons from In Vitro and Animal Models
Greg M. Cole,Takashi Morihara,Takashi Morihara,Giselle P. Lim,Giselle P. Lim,Fusheng Yang,Fusheng Yang,Aynun N. Begum,Aynun N. Begum,Sally A. Frautschy +9 more
TL;DR: At sustainable doses designed to mimic protective consumption in the epidemiology, ibuprofen reduces amyloid accumulation but suppresses a surprisingly limited subset of inflammatory markers in APPsw transgenic mice.
Journal ArticleDOI
Increased production of inflammatory cytokines in mild cognitive impairment.
TL;DR: The data indicate that changes in cytokine production by PBMCs may be detected early in MCI, and an alteration of the immune response may precede clinical AD.
Journal ArticleDOI
Neuroprotective Effect of Fisetin Against Amyloid-Beta-Induced Cognitive/Synaptic Dysfunction, Neuroinflammation, and Neurodegeneration in Adult Mice
TL;DR: It is suggested that fisetin has a potent neuroprotective effect against Aβ1–42-induced neurotoxicity and demonstrated that polyphenolic flavonoids such as f isetin could be a beneficial, effective and safe neuroProtective agent for preventing neurological disorders such as AD.
Journal ArticleDOI
α-1-Antichymotrypsin Promotes β-Sheet Amyloid Plaque Deposition in a Transgenic Mouse Model of Alzheimer's Disease
Lars N.G. Nilsson,Kelly R. Bales,Giovanni DiCarlo,Marcia N. Gordon,Dave Morgan,Steven M. Paul,Huntington Potter +6 more
TL;DR: The data demonstrate that ACT promotes amyloid deposition and provide a specific mechanism by which inflammation and the subsequent upregulation of astrocytic ACT expression in AD brain contributes to AD pathogenesis.
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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