From Charcot to SOD1 Mechanisms of Selective Motor Neuron Death in ALS
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[1] Ole A. Andreassen,et al. Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis , 1999, Nature Medicine.
[2] Y. Itoyama,et al. Selective impairment of fast anterograde axonal transport in the peripheral nerves of asymptomatic transgenic mice with a G93A mutant SOD1 gene , 1999, Brain Research.
[3] A Al-Chalabi,et al. Deletions of the heavy neurofilament subunit tail in amyotrophic lateral sclerosis. , 1999, Human molecular genetics.
[4] Wendy Bruening,et al. Up‐Regulation of Protein Chaperones Preserves Viability of Cells Expressing Toxic Cu/Zn‐Superoxide Dismutase Mutants Associated with Amyotrophic Lateral Sclerosis , 1999, Journal of neurochemistry.
[5] J. Slade,et al. Novel insertion in the KSP region of the neurofilament heavy gene in amyotrophic lateral sclerosis (ALS) , 1998, Neuroreport.
[6] M. Gurney,et al. Protein Oxidative Damage in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis , 1998, Journal of neurochemistry.
[7] L. Bruijn,et al. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. , 1998, Science.
[8] Q. Zhu,et al. Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[9] Q. Zhu,et al. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[10] R. Mason,et al. Reexamination of the mechanism of hydroxyl radical adducts formed from the reaction between familial amyotrophic lateral sclerosis-associated Cu,Zn superoxide dismutase mutants and H2O2. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[11] V. Culotta,et al. Chaperone-facilitated copper binding is a property common to several classes of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[12] Y. Itoyama,et al. Identification of alternative splicing forms of GLT-1 mRNA in the spinal cord of amyotrophic lateral sclerosis patients , 1998, Neuroscience Letters.
[13] Lin Jin,et al. Aberrant RNA Processing in a Neurodegenerative Disease: the Cause for Absent EAAT2, a Glutamate Transporter, in Amyotrophic Lateral Sclerosis , 1998, Neuron.
[14] Robert H. Brown,et al. Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis , 1997, Journal of neurochemistry.
[15] R. Casareno,et al. The Copper Chaperone for Superoxide Dismutase* , 1997, The Journal of Biological Chemistry.
[16] M. Dubois‐Dauphin,et al. Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. , 1997, Science.
[17] D. Price,et al. Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[18] Junying Yuan,et al. Inhibition of ICE slows ALS in mice , 1997, Nature.
[19] D. Figlewicz,et al. Aggregation of Mutant Cu/Zn Superoxide Dismutase Proteins in a Culture Model of ALS , 1997, Journal of neuropathology and experimental neurology.
[20] D. Borchelt,et al. ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions , 1997, Neuron.
[21] H. Horvitz,et al. Epidemiology of mutations in superoxide dismutase in amyotrophic lateal sclerosis , 1997, Annals of neurology.
[22] P. Leigh,et al. Dose-ranging study of riluzole in amyotrophic lateral sclerosis , 1996, The Lancet.
[23] M. Beal,et al. Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury , 1996, Nature Genetics.
[24] M. Gurney,et al. Benefit of vitamin E, riluzole, and gababapentin in a transgenic model of familial amyotrophic lateral sclerosis , 1996, Annals of neurology.
[25] D. Bredesen,et al. Altered Reactivity of Superoxide Dismutase in Familial Amyotrophic Lateral Sclerosis , 1996, Science.
[26] A. Levey,et al. Selective loss of glial glutamate transporter GLT‐1 in amyotrophic lateral sclerosis , 1995, Annals of neurology.
[27] D. Borchelt,et al. An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria , 1995, Neuron.
[28] Robert H. Brown,et al. Amyotrophic lateral sclerosis: Recent insights from genetics and transgenic mice , 1995, Cell.
[29] J. Morrison,et al. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[30] V. Meininger,et al. Variants of the heavy neurofilament subunit are associated with the development of amyotrophic lateral sclerosis. , 1994, Human molecular genetics.
[31] D. Borchelt,et al. Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[32] M. Gurney,et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. , 1994, Science.
[33] Robert H. Brown,et al. Superoxide Dismutase Activity, Oxidative Damage, and Mitochondrial Energy Metabolism in Familial and Sporadic Amyotrophic Lateral Sclerosis , 1993, Journal of neurochemistry.
[34] M. Carson,et al. ALS, SOD and peroxynitrite , 1993, Nature.
[35] J. Haines,et al. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis , 1993, Nature.
[36] L. Kurland,et al. Fine Structural Study of Neurofibrillary Changes in a Family with Amyotrophic Lateral Sclerosis , 1984, Journal of neuropathology and experimental neurology.
[37] A. Hirano,et al. Fine Structural Observations of Neurofilamentous Changes in Amyotrophic Lateral Sclerosis , 1984, Journal of neuropathology and experimental neurology.
[38] P. Dyck,et al. Morphometric Comparison of the Vulnerability of Peripheral Motor and Sensory Neurons in Amyotrophic Lateral Sclerosis , 1981, Journal of neuropathology and experimental neurology.
[39] A. F. Soleng,et al. A thorny question: how does activity maintain dendritic spines? , 1999, Nature Neuroscience.
[40] K. Narasimhan,et al. Signaling myopia , 1999, Nature Neuroscience.
[41] P. Leigh,et al. Dose-ranging study of riluzole in amyotrophic lateral sclerosis. Amyotrophic Lateral Sclerosis/Riluzole Study Group II. , 1996, Lancet.