Microglial Activation and Dopaminergic Cell Injury: An In Vitro Model Relevant to Parkinson's Disease
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Wenjie Xie | S. Appel | Stanley H. Appel | Yi He | Wei-dong Le | W. Xie | W. Le | Dominic Rowe | Irving Ortiz | Yi He | Dominic B. Rowe | I. Ortiz
[1] J. Merrill,et al. Cytokines in inflammatory brain lesions: helpful and harmful , 1996, Trends in Neurosciences.
[2] P. Damier,et al. Glial cells and inflammation in parkinson's disease: A role in neurodegeneration? , 1998, Annals of neurology.
[3] F. Rossi,et al. beta-amyloid activates the O-2 forming NADPH oxidase in microglia, monocytes, and neutrophils. A possible inflammatory mechanism of neuronal damage in Alzheimer's disease. , 1999, The Journal of biological chemistry.
[4] M. Beal,et al. Excitotoxicity and nitric oxide in parkinson's disease pathogenesis , 1998, Annals of neurology.
[5] K. Jellinger,et al. The pathology of Parkinson's disease. , 2001, Advances in neurology.
[6] J. Fazakerley,et al. Specific infection and destruction of dopaminergic neurons in the substantia nigra by Theiler's virus , 1997, Journal of virology.
[7] O. Hansson,et al. Improving the survival of grafted dopaminergic neurons: a review over current approaches. , 2000, Cell transplantation.
[8] W. Hall,et al. A rat model of Parkinson's disease induced by Japanese encephalitis virus. , 1997, Journal of neurovirology.
[9] T. Molitor,et al. Activated microglia mediate neuronal cell injury via a nitric oxide mechanism. , 1992, Journal of immunology.
[10] S. Shimohama,et al. Dopamine D2‐type agonists protect mesencephalic neurons from glutamate neurotoxicity: Mechanisms of neuroprotective treatment against oxidative stress , 1998, Annals of neurology.
[11] T. Montine,et al. Covalent Crosslinking of Neurofilament Proteins by Oxidized Catechols as a Potential Mechanism of Lewy Body Formation , 1995, Journal of neuropathology and experimental neurology.
[12] T. Nagatsu,et al. Interleukin (IL)-1 beta, IL-2, IL-4, IL-6 and transforming growth factor-alpha levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and Parkinson's disease. , 1996, Neuroscience letters.
[13] E. Hirsch,et al. FcεRII/CD23 Is Expressed in Parkinson’s Disease and Induces, In Vitro, Production of Nitric Oxide and Tumor Necrosis Factor-α in Glial Cells , 1999, The Journal of Neuroscience.
[14] E. Stefani,et al. Serum antibodies to L-type calcium channels in patients with amyotrophic lateral sclerosis. , 1992, The New England journal of medicine.
[15] Ted M. Dawson,et al. Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson disease , 1999, Nature Medicine.
[16] J. Newcombe,et al. Low density lipoprotein uptake by macrophages in multiple sclerosis plaques: implications for pathogenesis , 1994, Neuropathology and applied neurobiology.
[17] W. Le,et al. Antibodies from patients with Parkinson's disease react with protein modified by dopamine oxidation , 1998, Journal of neuroscience research.
[18] T. Ørntoft,et al. Association of IgM type anti‐GM1 antibodies and muscle strength in chronic acquired demylelinating polyneuropathy , 1998, Annals of neurology.
[19] P. Mcgeer,et al. Reactive microglia are positive for HLA‐DR in the substantia nigra of Parkinson's and Alzheimer's disease brains , 1988, Neurology.
[20] S. Appel,et al. Experimental destruction of substantia nigra initiated by Parkinson disease immunoglobulins. , 1998, Archives of neurology.
[21] S. Appel,et al. Experimental autoimmune nigral damage in guinea pigs , 1995, Journal of Neuroimmunology.
[22] K. McNaught,et al. Altered Glial Function Causes Neuronal Death and Increases Neuronal Susceptibility to 1‐Methyl‐4‐Phenylpyridinium‐ and 6‐Hydroxydopamine‐Induced Toxicity in Astrocytic/Ventral Mesencephalic Co‐Cultures , 1999, Journal of neurochemistry.
[23] M. McMillian,et al. Role of Protein Kinase C in Microglia‐induced Neurotoxicity in Mesencephalic Cultures , 1997, Journal of neuropathology and experimental neurology.
[24] P. Jenner,et al. Understanding cell death in parkinson's disease , 1998, Annals of neurology.
[25] J. Ravetch,et al. FcR γ chain deletion results in pleiotrophic effector cell defects , 1994, Cell.
[26] E. Stefani,et al. A novel N18TG2 x mesencephalon cell hybrid expresses properties that suggest a dopaminergic cell line of substantia nigra origin , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[27] M. Mattson,et al. Oxidized lipoproteins increase reactive oxygen species formation in microglia and astrocyte cell lines , 1999, Brain Research.
[28] L. Colom,et al. Cell death induced by β-amyloid 1–40 in MES 23.5 hybrid clone: the role of nitric oxide and NMDA-gated channel activation leading to apoptosis , 1995, Brain Research.
[29] T. Nagatsu,et al. Interleukin (IL)-1β, IL-2, IL-4, IL-6 and transforming growth factor-α levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and Parkinson's disease , 1996, Neuroscience Letters.
[30] C. Marsden,et al. Increased levels of lipid hydroperoxides in the parkinsonian substantia nigra: An HPLC and ESR study , 1994 .
[31] G. Kreutzberg. Microglia: a sensor for pathological events in the CNS , 1996, Trends in Neurosciences.
[32] C. Marsden,et al. Increased levels of lipid hydroperoxides in the parkinsonian substantia nigra: An HPLC and ESR study , 1994, Movement disorders : official journal of the Movement Disorder Society.
[33] Haruhiko Akiyama,et al. Rate of cell death in parkinsonism indicates active neuropathological process , 1988, Annals of neurology.
[34] T. Saito,et al. FcR gamma-chain is essential for both surface expression and function of human Fc gamma RI (CD64) in vivo. , 1996, Blood.
[35] H. Wekerle,et al. Neuronal Control of the Immune Response in the Central Nervous System: Linking Brain Immunity to Neurodegeneration , 1998, Journal of neuropathology and experimental neurology.
[36] T. Montine,et al. Parkinson's disease is associated with oxidative damage to cytoplasmic DNA and RNA in substantia nigra neurons. , 1999, The American journal of pathology.
[37] J. Langston,et al. Evidence of active nerve cell degeneration in the substantia nigra of humans years after 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine exposure , 1999, Annals of neurology.
[38] A. Mayer. Therapeutic implications of microglia activation by lipopolysaccharide and reactive oxygen species generation in septic shock and central nervous system pathologies: a review. , 1998, Medicina.
[39] J. Jankovic,et al. Effects of cerebrospinal fluid from patients with Parkinson disease on dopaminergic cells. , 1999, Archives of neurology.
[40] B. Wainer,et al. In vitro cell cultures as a model of the basal forebrain. , 1991, Advances in experimental medicine and biology.
[41] J. Tajti,et al. Nigral damage and dopaminergic hypofunction in mesencephalon‐immunized guinea pigs , 1992, Annals of neurology.
[42] V. Perry,et al. Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain , 1990, Neuroscience.
[43] C. Marsden,et al. Mitochondrial Complex I Deficiency in Parkinson's Disease , 1990, Lancet.
[44] N. Hattori,et al. Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson disease. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[45] J. Cano,et al. Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System , 1998, Journal of neurochemistry.
[46] Minoru Harada,et al. Tumor necrosis factor-α (TNF-α) increases both in the brain and in the cerebrospinal fluid from parkinsonian patients , 1994, Neuroscience Letters.
[47] K. Jellinger,et al. Pathology of Parkinson's disease. Changes other than the nigrostriatal pathway. , 1991, Molecular and chemical neuropathology.
[48] A. H. V. Schapira,et al. MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE , 1989, The Lancet.