Inflammation, autotoxicity and Alzheimer disease

[1]  P. Mcgeer,et al.  Polymorphisms in inflammatory genes and the risk of Alzheimer disease. , 2001, Archives of neurology.

[2]  S. Webster,et al.  Antibody-Mediated Phagocytosis of the Amyloid β-Peptide in Microglia Is Differentially Modulated by C1q1 , 2001, The Journal of Immunology.

[3]  M. Staufenbiel,et al.  Comparative Analysis of Amyloid-β Chemical Structure and Amyloid Plaque Morphology of Transgenic Mouse and Alzheimer's Disease Brains* , 2001, The Journal of Biological Chemistry.

[4]  P. Mcgeer,et al.  Generation of C-reactive protein and complement components in atherosclerotic plaques. , 2001, The American journal of pathology.

[5]  W. Richards,et al.  Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.

[6]  P. Mcgeer,et al.  Reduced neprilysin in high plaque areas of Alzheimer brain: a possible relationship to deficient degradation of β-amyloid peptide , 2001, Neuroscience Letters.

[7]  A. Morelli,et al.  Nitric Oxide—Releasing NSAIDs , 2001, Drug safety.

[8]  P. Mcgeer,et al.  Human neurons generate C-reactive protein and amyloid P: upregulation in Alzheimer’s disease , 2000, Brain Research.

[9]  M. Albert,et al.  Association of a haplotype for tumor necrosis factor in siblings with late-onset Alzheimer disease: the NIMH Alzheimer Disease Genetics Initiative. , 2000, American journal of medical genetics.

[10]  G. Rebeck.  Confirmation of the genetic association of interleukin-1A with early onset sporadic Alzheimer's disease , 2000, Neuroscience Letters.

[11]  Rena Li,et al.  Deficiency of Complement Defense Protein CD59 May Contribute to Neurodegeneration in Alzheimer's Disease , 2000, The Journal of Neuroscience.

[12]  H J Koch,et al.  A randomized controlled trial of prednisone in Alzheimer’s disease , 2000, Neurology.

[13]  J. Rogers,et al.  Detection of complement alternative pathway mRNA and proteins in the Alzheimer's disease brain. , 2000, Brain research. Molecular brain research.

[14]  G. Annoni,et al.  Gene polymorphism affecting α1‐antichymotrypsin and interleukin‐1 plasma levels increases Alzheimer's disease risk , 2000, Annals of neurology.

[15]  M. Citron,et al.  Aβ-Generating Enzymes Recent Advances in β- and γ-Secretase Research , 2000, Neuron.

[16]  W. Oertel,et al.  Association of an interleukin 1α polymorphism with Alzheimer’s disease , 2000, Neurology.

[17]  P. Mcgeer.  Cyclo-Oxygenase-2 Inhibitors , 2000, Drugs & aging.

[18]  J. Schwab,et al.  Selective accumulation of cyclooxygenase-1-expressing microglial cells/macrophages in lesions of human focal cerebral ischemia , 2000, Acta Neuropathologica.

[19]  P. Mcgeer,et al.  Autotoxicity and Alzheimer disease. , 2000, Archives of neurology.

[20]  Robert B Sim,et al.  Complement C1q Is Dramatically Up-Regulated in Brain Microglia in Response to Transient Global Cerebral Ischemia1 2 , 2000, The Journal of Immunology.

[21]  A. Hofman,et al.  Duration of non-steroidal anti-inflammatory drug use and risk of Alzheimer's disease. The Rotterdam study , 2000, Neurobiology of Aging.

[22]  C. Plata-salamán,et al.  Inflammation and Alzheimer’s disease , 2000, Neurobiology of Aging.

[23]  L. Murray,et al.  Association of interleukin‐1 gene polymorphisms with Alzheimer's disease , 2000, Annals of neurology.

[24]  Association of early‐onset Alzheimer's disease with an interleukin‐1α gene polymorphism , 2000, Annals of neurology.

[25]  K. Davis,et al.  A randomized controlled trial of prednisone in Alzheimer’s disease , 2000, Neurology.

[26]  T. Saido,et al.  Identification of the major Aβ1–42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition , 2000, Nature Medicine.

[27]  A. Bernstein,et al.  Mice lacking both presenilin genes exhibit early embryonic patterning defects. , 1999, Genes & development.

[28]  J. Rogers,et al.  Cyclooxygenase-1 in human Alzheimer and control brain: quantitative analysis of expression by microglia and CA3 hippocampal neurons. , 1999, Journal of neuropathology and experimental neurology.

[29]  J. Treanor,et al.  Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.

[30]  B. Strooper,et al.  Presenilin-1 deficiency leads to loss of Cajal–Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly , 1999, Current Biology.

[31]  R. Motter,et al.  Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse , 1999, Nature.

[32]  C. Visser,et al.  C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? , 1999, Circulation.

[33]  P. Mcgeer,et al.  Complement regulators C1 inhibitor and CD59 do not significantly inhibit complement activation in Alzheimer disease , 1999, Brain Research.

[34]  Šimon Scharf,et al.  A double-blind, placebo-controlled trial of diclofenac/misoprostol in Alzheimer’s disease , 1999, Neurology.

[35]  P. Mcgeer,et al.  Distribution of cyclooxygenase-1 and cyclooxygenase-2 mRNAs and proteins in human brain and peripheral organs , 1999, Brain Research.

[36]  F. Jessen,et al.  A genetic variation of the inflammatory cytokine interleukin‐6 delays the initial onset and reduces the risk for sporadic Alzheimer's disease , 1999, Annals of neurology.

[37]  K. Lees,et al.  C-reactive protein and outcome after ischemic stroke. , 1999, Stroke.

[38]  D. Selkoe,et al.  Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity , 1999, Nature.

[39]  P. Mcgeer,et al.  Up-regulated production and activation of the complement system in Alzheimer's disease brain. , 1999, The American journal of pathology.

[40]  A. Döring,et al.  C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. , 1999, Circulation.

[41]  G. Wenk,et al.  Peripheral administration of novel anti-inflammatories can attenuate the effects of chronic inflammation within the CNS , 1999, Brain Research.

[42]  P. Mcgeer,et al.  Human heart generates complement proteins that are upregulated and activated after myocardial infarction. , 1998, Circulation research.

[43]  W. Koenig,et al.  C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[44]  Steven M. Horvath,et al.  Alpha-2 macroglobulin is genetically associated with Alzheimer disease , 1998, Nature Genetics.

[45]  A. Akaike,et al.  Localization of fractalkine and CX3CR1 mRNAs in rat brain: does fractalkine play a role in signaling from neuron to microglia? , 1998, FEBS letters.

[46]  Gurparkash Singh,et al.  Mutant Human Presenilin 1 Protects presenilin 1 Null Mouse against Embryonic Lethality and Elevates Aβ1–42/43 Expression , 1998, Neuron.

[47]  P. Ridker,et al.  Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. , 1998, Circulation.

[48]  L. Lue,et al.  Molecular and Cellular Characterization of the Membrane Attack Complex, C5b-9, in Alzheimer’s Disease , 1997, Neurobiology of Aging.

[49]  A. Akaike,et al.  Induction of macrophage inflammatory protein MIP-1α mRNA on glial cells after focal cerebral ischemia in the rat , 1997, Neuroscience Letters.

[50]  A. Sauter,et al.  Differential and time-dependent expression of monocyte chemoattractant protein-1 mRNA by astrocytes and macrophages in rat brain: effects of ischemia and peripheral lipopolysaccharide administration , 1997, Journal of Neuroimmunology.

[51]  J. Haines,et al.  Re: Genetic effect of α1-antichymotrypsin on the risk of Alzheimer disease , 1997 .

[52]  W F Stewart,et al.  Risk of Alzheimer's disease and duration of NSAID use , 1997, Neurology.

[53]  C. Visser,et al.  C-reactive protein colocalizes with complement in human hearts during acute myocardial infarction. , 1997, Circulation.

[54]  A. Roher,et al.  Complement interactions with amyloid β1–42: A nidus for inflammation in AD brains , 1997 .

[55]  J. Rogers,et al.  Relative efficacies of amyloid β peptide (Aβ) binding proteins in Aβ aggregation , 1996 .

[56]  A. Pasternack,et al.  Serum C-reactive protein concentration in acute myocardial infarction and its relationship to mortality during 24 months of follow-up in patients under thrombolytic treatment. , 1996, European heart journal.

[57]  Patrick L. McGeer,et al.  Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease , 1996, Neurology.

[58]  K. Seibert,et al.  Cyclooxygenase-2 inhibitors: a new class of anti-inflammatory agents that spare the gastrointestinal tract. , 1996, Gastroenterology clinics of North America.

[59]  C. Glabe,et al.  Multivalent Binding of Complement Protein C1q to the Amyloid β-Peptide (Aβ) Promotes the Nucleation Phase of Aβ Aggregation , 1995 .

[60]  J. Johnston,et al.  Renal abnormalities and an altered inflammatory response in mice lacking cyclooxygenase II , 1995, Nature.

[61]  P. Mcgeer,et al.  The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases , 1995, Brain Research Reviews.

[62]  J. Wallace,et al.  Nitric oxide-releasing NSAIDs: a novel class of GI-sparing anti-inflammatory drugs. , 1995, Agents and actions. Supplements.

[63]  S. O’Barr,et al.  Enhanced aggregation and β structure of amyloid β peptide after coincubation with C1Q , 1994 .

[64]  P. Mcgeer,et al.  Ultrastructural localization of complement membrane attack complex (MAC)-like immunoreactivity in brains of patients with Alzheimer's disease , 1994, Brain Research.

[65]  R. Mangues,et al.  Brain interleukin-1 beta in Alzheimer's disease and vascular dementia. , 1994, Methods and findings in experimental and clinical pharmacology.

[66]  A. Whitehead,et al.  The major acute phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A protein. , 1994, Immunology today.

[67]  Paul L. Wood,et al.  Cytokine indices in Alzheimer's temporal cortex: no changes in mature IL-1β or IL-1RA but increases in the associated acute phase proteins IL-6, α2-macroglobulin and C-reactive protein , 1993, Brain Research.

[68]  A. Kaszniak,et al.  Clinical trial of indomethacin in Alzheimer's disease , 1993, Neurology.

[69]  S. Tomlinson.  Complement defense mechanisms. , 1993, Current opinion in immunology.

[70]  D. Dickson,et al.  Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease , 1993, Glia.

[71]  P. Mcgeer,et al.  Complement activation by beta-amyloid in Alzheimer disease. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[72]  W. Griffin,et al.  Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[73]  S. Styren,et al.  Expression of immune system-associated antigens by cells of the human central nervous system: Relationship to the pathology of Alzheimer's disease , 1988, Neurobiology of Aging.

[74]  P. Mcgeer,et al.  Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR , 1987, Neuroscience Letters.

[75]  W. A. Newman Dorland,et al.  Dorland's Illustrated Medical Dictionary , 1974 .

[76]  Elias Metschnikoff.  Leçons sur la pathologie comparée de l'inflammation , 1893 .