Altered calcium homeostasis in ALS as a target for therapy.

[1]  I. Kanazawa,et al.  Reduction of GluR2 RNA editing, a molecular change that increases calcium influx through AMPA receptors, selective in the spinal ventral gray of patients with amyotrophic lateral sclerosis , 1999, Annals of neurology.

[2]  D. Cleveland.  From Charcot to SOD1 Mechanisms of Selective Motor Neuron Death in ALS , 1999, Neuron.

[3]  Margaret A. Johnson,et al.  Mitochondrial enzyme activity in amyotrophic lateral sclerosis: Implications for the role of mitochondria in neuronal cell death , 1999, Annals of neurology.

[4]  R. Adalbert,et al.  Calcium-containing endosomes at oculomotor terminals in animal models of ALS. , 1999, Neuroreport.

[5]  P. Leigh,et al.  Cells from individuals with SOD-1 associated familial amyotrophic lateral sclerosis do not have an increased susceptibility to radiation-induced free radical production or DNA damage , 1999, Journal of the Neurological Sciences.

[6]  J. Slade,et al.  Low expression of GluR2 AMPA receptor subunit protein by human motor neurons. , 1999, Neuroreport.

[7]  D. Figlewicz,et al.  Glutamate Potentiates the Toxicity of Mutant Cu/Zn-Superoxide Dismutase in Motor Neurons by Postsynaptic Calcium-Dependent Mechanisms , 1998, The Journal of Neuroscience.

[8]  M. Mattson,et al.  Protein modification by the lipid peroxidation product 4‐hydroxynonenal in the spinal cords of amyotrophic lateral sclerosis patients , 1998, Annals of neurology.

[9]  M. Mattson,et al.  Presence of 4‐hydroxynonenal in cerebrospinal fluid of patients with sporadic amyotrophic lateral sclerosis , 1998, Annals of neurology.

[10]  S. Sensi,et al.  Rapid Ca2+ Entry through Ca2+-Permeable AMPA/Kainate Channels Triggers Marked Intracellular Ca2+Rises and Consequent Oxygen Radical Production , 1998, The Journal of Neuroscience.

[11]  Gary L. Pattee,et al.  Mitochondria in Sporadic Amyotrophic Lateral Sclerosis , 1998, Experimental Neurology.

[12]  J. Morrison,et al.  Light and electron microscopic distribution of the AMPA receptor subunit, GluR2, in the spinal cord of control and G86R mutant superoxide dismutase transgenic mice , 1998, The Journal of comparative neurology.

[13]  M. Gurney,et al.  Intracellular Calcium Parallels Motoneuron Degeneration in SOD-1 Mutant Mice , 1998, Journal of neuropathology and experimental neurology.

[14]  W. Robberecht,et al.  Increased sensitivity of fibroblasts from amyotrophic lateral sclerosis patients to oxidative stress , 1998, Annals of neurology.

[15]  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.

[16]  W. Kunz,et al.  Impairment of mitochondrial function in skeletal muscle of patients with amyotrophic lateral sclerosis , 1998, Journal of the Neurological Sciences.

[17]  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.

[18]  M. Mattson,et al.  4‐hydroxynonenal, a lipid peroxidation product, impairs glutamate transport in cortical astrocytes , 1998, Glia.

[19]  S. Appel,et al.  1α, 25 dihydroxyvitamin D3‐dependent up‐regulation of calcium‐binding proteins in motoneuron cells , 1998 .

[20]  C. M. Hansen,et al.  EB 1089, a novel vitamin D analog with strong antiproliferative and differentiation-inducing effects on target cells. , 1997, Biochemical pharmacology.

[21]  Robert H. Brown,et al.  Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis , 1997, Journal of neurochemistry.

[22]  Robert H. Brown,et al.  Increased 3‐nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis , 1997, Annals of neurology.

[23]  F. Poccia,et al.  Expression of a Cu,Zn superoxide dismutase typical of familial amyotrophic lateral sclerosis induces mitochondrial alteration and increase of cytosolic Ca2+ concentration in transfected neuroblastoma SH‐SY5Y cells , 1997, FEBS letters.

[24]  L. Colom,et al.  Amyotrophic Lateral Sclerosis Immunoglobulins Increase Intracellular Calcium in a Motoneuron Cell Line , 1997, Experimental Neurology.

[25]  J M Land,et al.  Nitric Oxide‐Mediated Mitochondrial Damage in the Brain: Mechanisms and Implications for Neurodegenerative Diseases , 1997, Journal of neurochemistry.

[26]  S. Appel,et al.  Altered Calcium Homeostasis and Ultrastructure in Motoneurons of Mice Caused by Passively Transferred Anti‐motoneuronal IgG , 1997, Journal of neuropathology and experimental neurology.

[27]  M. Dehouck,et al.  1,25-dihydroxyvitamin D3 regulates γ-glutamyl transpeptidase activity in rat brain , 1996, Neuroscience Letters.

[28]  Y. Nagata,et al.  Decreased cytochrome c oxidase activity but unchanged superoxide dismutase and glutathione peroxidase activities in the spinal cords of patients with amyotrophic lateral sclerosis , 1996, Journal of neuroscience research.

[29]  P. Brachet,et al.  1,25 Dihydroxyvitamin D3 Exerts Regional Effects in the Central Nervous System during Experimental Allergic Encephalomyelitis , 1996, Journal of neuropathology and experimental neurology.

[30]  J. Weiss,et al.  Motor Neurons Are Selectively Vulnerable to AMPA/Kainate Receptor-Mediated Injury In Vitro , 1996, The Journal of Neuroscience.

[31]  L. Colom,et al.  Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[32]  E. Stadtman,et al.  A gain-of-function of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant: An enhancement of free radical formation due to a decrease in Km for hydrogen peroxide. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[33]  P. Leigh,et al.  Dose-ranging study of riluzole in amyotrophic lateral sclerosis , 1996, The Lancet.

[34]  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.

[35]  M. Hediger,et al.  Knockout of Glutamate Transporters Reveals a Major Role for Astroglial Transport in Excitotoxicity and Clearance of Glutamate , 1996, Neuron.

[36]  M. Gurney,et al.  Benefit of vitamin E, riluzole, and gababapentin in a transgenic model of familial amyotrophic lateral sclerosis , 1996, Annals of neurology.

[37]  F. Joó,et al.  Ultrastructural evidence for altered calcium in motor nerve terminals in amyotrophc lateral sclerosis , 1996, Annals of neurology.

[38]  G. Rosoklija,et al.  Brain superoxide dismutase, catalase, and glutathione peroxidase activities in amyotrophic lateral sclerosis , 1996, Annals of neurology.

[39]  M. Goldberg,et al.  Mitochondrial production of reactive oxygen species in cortical neurons following exposure to N-methyl-D-aspartate , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[40]  P. Ince,et al.  Oxidative damage to protein in sporadic motor neuron disease spinal cord , 1995, Annals of neurology.

[41]  A. Levey,et al.  Selective loss of glial glutamate transporter GLT‐1 in amyotrophic lateral sclerosis , 1995, Annals of neurology.

[42]  L. Komuves,et al.  Antibodies to calcium channels from ALS patients passively transferred to mice selectively increase intracellular calcium and induce ultrastructural changes in motoneurons , 1995, Synapse.

[43]  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.

[44]  R. Bouillon,et al.  Structure-function relationships in the vitamin D endocrine system. , 1995, Endocrine reviews.

[45]  T. Yamaguchi,et al.  The effect of insulin and insulin-like growth factor-1 on the expression of calretinin and calbindin D-28k in rat embryonic neurons in culture , 1995, Neurochemistry International.

[46]  E. Stefani,et al.  Amyotrophic lateral sclerosis immunoglobulins increase Ca2+ currents in a motoneuron cell line , 1995, Annals of neurology.

[47]  V. La Bella,et al.  The role of calcium‐binding proteins in selective motoneuron vulnerability in amyotrophic lateral sclerosis , 1994, Annals of neurology.

[48]  M. Gurney,et al.  Development of central nervous system pathology in a murine transgenic model of human amyotrophic lateral sclerosis. , 1994, The American journal of pathology.

[49]  W. D. Ehmann,et al.  Iron, selenium and glutathione peroxidase activity are elevated in sporadic motor neuron disease , 1994, Neuroscience Letters.

[50]  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.

[51]  J. Dykens.  Isolated Cerebral and Cerebellar Mitochondria Produce Free Radicals when Exposed to Elevated Ca2+ and Na+: Implications for Neurodegeneration , 1994, Journal of neurochemistry.

[52]  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.

[53]  J. Coyle,et al.  Oxidative stress, glutamate, and neurodegenerative disorders. , 1993, Science.

[54]  Joseph Loscalzo,et al.  A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds , 1993, Nature.

[55]  J. Rothstein,et al.  Chronic inhibition of glutamate uptake produces a model of slow neurotoxicity. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[56]  Charles Tator,et al.  Source specificity of early calcium neurotoxicity in cultured embryonic spinal neurons , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[57]  S. Appel.  Excitotoxic neuronal cell death in amyotrophic lateral sclerosis , 1993, Trends in Neurosciences.

[58]  P. Emson,et al.  Stable transfection of calbindin-D28k into the GH3 cell line alters calcium currents and intracellular calcium homeostasis , 1992, Neuron.

[59]  J. D. Macklis,et al.  Calcium‐mediated neuronal degeneration following singlet oxygen production , 1992, Neuroreport.

[60]  C. Heizmann,et al.  Changes in Ca2+-binding proteins in human neurodegenerative disorders , 1992, Trends in Neurosciences.

[61]  J. Rothstein,et al.  Decreased glutamate transport by the brain and spinal cord in amyotrophic lateral sclerosis. , 1992, The New England journal of medicine.

[62]  S. Christakos,et al.  Nerve growth factor increases calcium binding protein (Calbindin-D28K) in rat olfactory bulb , 1992, Brain Research.

[63]  S. Mehrotra,et al.  Interrelation of active oxygen species, membrane damage and altered calcium functions , 1992, Molecular and Cellular Biochemistry.

[64]  A. C. Maiyar,et al.  1,25(OH)2-vitamin D3, a steroid hormone that produces biologic effects via both genomic and nongenomic pathways , 1992, The Journal of Steroid Biochemistry and Molecular Biology.

[65]  A. Norman,et al.  Monoclonal antibodies directed against the calcium binding protein Calbindin D-28k. , 1990, Cell calcium.

[66]  J. Coyle,et al.  Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis , 1990, Annals of neurology.

[67]  S. Maruyama,et al.  Ultrastructure of swollen proximal axons of anterior horn neurons in motor neuron disease , 1990, Journal of the Neurological Sciences.

[68]  S. Orrenius,et al.  Role of Ca2+ in toxic cell killing. , 1989, Trends in pharmacological sciences.

[69]  A. Tashjian,et al.  Dual actions of 1,25-dihydroxycholecalciferol on intracellular Ca2+ in GH4C1 cells: evidence for effects on voltage-operated Ca2+ channels and Na+/Ca2+ exchange. , 1989, Endocrinology.

[70]  K. Haglid,et al.  Parvalbumin increases in the caudate putamen of rats with vitamin D hypervitaminosis. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[71]  A. Norman,et al.  1,25(OH)2‐Vitamin D3 receptors: gene regulation and genetic circuitry , 1988, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[72]  D. Choi,et al.  Glutamate neurotoxicity and diseases of the nervous system , 1988, Neuron.

[73]  C. Gerday,et al.  Monoclonal antibodies directed against the calcium binding protein parvalbumin. , 1988, Cell calcium.

[74]  M. Haussler,et al.  Immunocytochemical localization of the 1,25-dihydroxyvitamin D3 receptor in target cells. , 1988, Endocrinology.

[75]  W. Stumpf,et al.  1,25(OH)2 vitamin D3 sites of action in the brain , 1987, Histochemistry.

[76]  M. Mattson,et al.  Roles of Lipid Peroxidation in Modulation of Cellular Signaling Pathways, Cell Dysfunction, and Death in the Nervous System , 1998, Reviews in the neurosciences.

[77]  M. Chen,et al.  Increased sensitivity of , 1998 .

[78]  K. Hirayama,et al.  Hepatic ultrastructural changes and liver dysfunction in amyotrophic lateral sclerosis. , 1987, Archives of neurology.