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B. Bradt, W. Kolb, N. Cooper (1998)
Complement-dependent Proinflammatory Properties of the Alzheimer's Disease β-PeptideThe Journal of Experimental Medicine, 188
B. Morgan, P. Gasque (1996)
Expression of complement in the brain: role in health and disease.Immunology today, 17 10
E. Benveniste (1992)
Inflammatory cytokines within the central nervous system: sources, function, and mechanism of action.The American journal of physiology, 263 1 Pt 1
J. Rogers, S. O’Barr (1997)
Inflammatory Mediators in Alzheimer’s Disease
Scott Webster, Barry Bonnell, Joseph Rogers (1997)
Charge-based binding of complement component C1q to the Alzheimer amyloid beta-peptide.The American journal of pathology, 150 5
P. Mcgeer, E. Mcgeer (1995)
The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseasesBrain Research Reviews, 21
P. Mcgeer, E. Mcgeer (1999)
Inflammation of the brain in Alzheimer's disease: implications for therapyJournal of Leukocyte Biology, 65
P. Velázquez, D. Cribbs, T. Poulos, A. Tenner (1997)
Aspartate residue 7 in amyloid β-protein is critical for classical complement pathway activation: Implications for Alzheimer's disease pathogenesisNature Medicine, 3
J Rogers, S O'Barr (1997)
Molecular Mechanisms of Dementia
L. Lue, L. Brachova, Harold Civin, J. Rogers (1996)
Inflammation, A beta deposition, and neurofibrillary tangle formation as correlates of Alzheimer's disease neurodegeneration.Journal of neuropathology and experimental neurology, 55 10
D. Games, David Adams, Ree Alessandrini, R. Barbour, Patricia Borthelette, C. Blackwell, Tony Carr, J. Clemens, T. Donaldson, F. Gillespie, T. Guido, S. Hagopian, K. Johnson-wood, K. Khan, Mike Lee, P. Leibowitz, I. Lieberburg, S. Little, E. Masliah, L. McConlogue, M. Montoya-Zavala, L. Mucke, L. Paganini, E. Penniman, M. Power, D. Schenk, P. Seubert, B. Snyder, F. Soriano, H. Tan, J. Vitale, S. Wadsworth, B. Wolozin, Jun Zhao (1995)
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor proteinNature, 373
K. Hsiao, P. Chapman, S. Nilsen, C. Eckman, Y. Harigaya, S. Younkin, Fusheng Yang, G. Cole (1996)
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic MiceScience, 274
S. Arnold, B. Hyman, J. Flory, A. Damasio, G. Hoesen (1991)
The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer's disease.Cerebral cortex, 1 1
Haixiang Jiang, D. Burdick, C. Glabe, C. Cotman, A. Tenner (1994)
beta-Amyloid activates complement by binding to a specific region of the collagen-like domain of the C1q A chain.Journal of immunology, 152 10
NR Cooper (1997)
Inflammation: Basic Principles and Clinical Correlates
J. Boer, G. Wolbink, L. Thijs, J. Baars, J. Wagstaff, C. Hack (1992)
Interplay of complement and cytokines in the pathogenesis of septic shock.Immunopharmacology, 24 2
K. Yasojima, C. Schwab, E. Mcgeer, P. Mcgeer (1999)
Up-regulated production and activation of the complement system in Alzheimer's disease brain.The American journal of pathology, 154 3
J. Rogers, N. Cooper, S. Webster, J. Schultz, P. Mcgeer, S. Styren, W. Civin, L. Brachova, B. Bradt, P. Ward (1992)
Complement activation by beta-amyloid in Alzheimer disease.Proceedings of the National Academy of Sciences of the United States of America, 89 21
P Eikelenboom, FC Stam (1982)
Immunoglobulins and complement factors in senile plaquesActa Neuropathol, 57
We hypothesize that amyloid (Aβ) peptide-containing neuritic plaques in the brains of patients with Alzheimer's disease represent chronic inflammatory foci mediated by the actions of the complement system and proinflammatory cytokines. In support of this, in vitro studies show that the (Aβ) peptide is a potent complement activator and that such complement activation leads to the formation of covalent (Aβ)-C3 activation fragment complexes, the generation of the chemokine-like C5a complement activation peptide, and the formation of the proinflammatory C5b-9 complex in functionally active form able to insert into neuronal cell membranes. Other studies show that C5a, together with (Aβ), synergistically augments the release of proinflammatory cytokines from human monocytes. These studies, which provide in vitro support for the hypothesis, are being pursued in an animal model of Alzheimer's disease.
Immunologic Research – Springer Journals
Published: Apr 25, 2007
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