Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice
暂无分享,去创建一个
John D Lambris | E. Masliah | T. Wyss-Coray | J. Lambris | J. Alexander | R. Quigg | F. Yan | A. Lin
[1] D. Coppola,et al. Microglial Activation and β-Amyloid Deposit Reduction Caused by a Nitric Oxide-Releasing Nonsteroidal Anti-Inflammatory Drug in Amyloid Precursor Protein Plus Presenilin-1 Transgenic Mice , 2002, The Journal of Neuroscience.
[2] C. Abraham. Reactive astrocytes and α1-antichymotrypsin in Alzheimer’s disease ☆ ☆ Supported by the NIH and the Alzheimer’s Association. , 2001, Neurobiology of Aging.
[3] O. Lindvall,et al. Stereological assessment of vulnerability of immunocytochemically identified striatal and hippocampal neurons after global cerebral ischemia in rats , 2001, Brain Research.
[4] Z. Fishelson,et al. Complement and apoptosis. , 2001, Molecular immunology.
[5] Virginia M. Y. Lee,et al. Complement activation by neurofibrillary tangles in Alzheimer's disease , 2001, Neuroscience Letters.
[6] L. Mucke,et al. TGF-β1 promotes microglial amyloid-β clearance and reduces plaque burden in transgenic mice , 2001, Nature Medicine.
[7] John D Lambris,et al. Structure and biology of complement protein C3, a connecting link between innate and acquired immunity , 2001, Immunological reviews.
[8] C. Lemere,et al. Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease. , 2001, The American journal of pathology.
[9] Brian J. Bacskai,et al. Imaging of amyloid-β deposits in brains of living mice permits direct observation of clearance of plaques with immunotherapy , 2001, Nature Medicine.
[10] E. Lavi,et al. Cutting Edge: C3, a Key Component of Complement Activation, Is Not Required for the Development of Myelin Oligodendrocyte Glycoprotein Peptide-Induced Experimental Autoimmune Encephalomyelitis in Mice1 , 2001, The Journal of Immunology.
[11] J. Hardy,et al. Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease , 2000, Nature.
[12] Ralph A. Nixon,et al. Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease , 2000, Nature.
[13] P. Gasque,et al. Complement components of the innate immune system in health and disease in the CNS. , 2000, Immunopharmacology.
[14] J. Lambris,et al. Complement and innate immunity. , 2000, Immunopharmacology.
[15] R. Motter,et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease , 2000, Nature Medicine.
[16] M. Emmerling,et al. The role of complement in Alzheimer's disease pathology. , 2000, Biochimica et biophysica acta.
[17] Kang Hu,et al. High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.
[18] C. Plata-salamán,et al. Inflammation and Alzheimer’s disease , 2000, Neurobiology of Aging.
[19] B. Palanca,et al. A critical role for murine complement regulator crry in fetomaternal tolerance. , 2000, Science.
[20] N. Davoust,et al. Central nervous system-targeted expression of the complement inhibitor sCrry prevents experimental allergic encephalomyelitis. , 1999, Journal of immunology.
[21] M. Svensson,et al. Glial responses to synaptic damage and plasticity , 1999, Journal of neuroscience research.
[22] N. Davoust,et al. Complement anaphylatoxin receptors on neurons: new tricks for old receptors? , 1999, Trends in Neurosciences.
[23] R. Motter,et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse , 1999, Nature.
[24] D. Giulian. Microglia and the immune pathology of Alzheimer disease. , 1999, American Journal of Human Genetics.
[25] D. Selkoe,et al. Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.
[26] D. Collier,et al. Stereological estimation of the total number of neurons in the murine hippocampus using the optical disector , 1999, The Journal of comparative neurology.
[27] Sarah Tomlin,et al. Microtechnology: Laying it on thick , 1999, Nature.
[28] R. Macdonald,et al. Renal, central nervous system and pancreatic overexpression of recombinant soluble Crry in transgenic mice. A novel means of protection from complement-mediated injury. , 1999, Immunopharmacology.
[29] P. Mcgeer,et al. Inflammation of the brain in Alzheimer's disease: implications for therapy , 1999, Journal of leukocyte biology.
[30] J. Alexander,et al. Transgenic Mice Overexpressing the Complement Inhibitor Crry as a Soluble Protein Are Protected from Antibody-induced Glomerular Injury , 1998, The Journal of experimental medicine.
[31] B. Bradt,et al. Complement-dependent Proinflammatory Properties of the Alzheimer's Disease β-Peptide , 1998, Journal of Experimental Medicine.
[32] Pier Paolo Pandolfi,et al. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies , 1998, Nature Genetics.
[33] David Garrick,et al. Repeat-induced gene silencing in mammals , 1998, Nature Genetics.
[34] J. Rogers,et al. Aggregation State‐Dependent Activation of the Classical Complement Pathway by the Amyloid β Peptide , 1997, Journal of neurochemistry.
[35] R. Motter,et al. Amyloid precursor protein processing and Aβ42 deposition in a transgenic mouse model of Alzheimer disease , 1997 .
[36] A. Roher,et al. Complement interactions with amyloid β1–42: A nidus for inflammation in AD brains , 1997 .
[37] L. Lue,et al. 735 Molecular, immunohistochemical, and ultrastructural characterization of complement proteins, including C5b-9, in ALZHEIMER'S disease , 1996, Neurobiology of Aging.
[38] Douglas Walker,et al. Inflammation and Alzheimer's disease pathogenesis , 1996, Neurobiology of Aging.
[39] M. Baudry,et al. Hereditary Deficiencies in Complement C5 Are Associated with Intensified Neurodegenerative Responses That Implicate New Roles for the C-System in Neuronal and Astrocytic Functions , 1996, Neurobiology of Disease.
[40] P. Anderson. Clinical Immunology: Principles and Practice , 1996 .
[41] A. Mccarthy. Development , 1996, Current Opinion in Neurobiology.
[42] L. Mucke,et al. Synaptotrophic effects of human amyloid β protein precursors in the cortex of transgenic mice , 1994, Brain Research.
[43] C. Cotman,et al. beta-Amyloid activates complement by binding to a specific region of the collagen-like domain of the C1q A chain. , 1994, Journal of immunology.
[44] 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.
[45] R. J. Mullen,et al. NeuN, a neuronal specific nuclear protein in vertebrates. , 1992, Development.
[46] G. Cole,et al. Phagocytosis and deposition of vascular beta-amyloid in rat brains injected with Alzheimer beta-amyloid. , 1992, The American journal of pathology.
[47] V. Holers,et al. Distinct receptor and regulatory properties of recombinant mouse complement receptor 1 (CR1) and Crry, the two genetic homologues of human CR1 , 1992, The Journal of experimental medicine.