CoChat
Sign Up
Cited by 127

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Mechanisms of glutamate toxicity in multiple sclerosis: biomarker and therapeutic opportunities

Macrez, Richard, Stys, Peter K, Vivien, Denis, Lipton, Stuart A, Docagne, Fabian·2016·The Lancet Neurology
DOI 10.1016/s1474-4422(16)30165-x
Open this paper in CoChat — free account

Abstract

Research advances support the idea that excessive activation of the glutamatergic pathway plays an important part in the pathophysiology of multiple sclerosis. Beyond the well established direct toxic effects on neurons, additional sites of glutamate-induced cell damage have been described, including effects in oligodendrocytes, astrocytes, endothelial cells, and immune cells. Such toxic effects could provide a link between various pathological aspects of multiple sclerosis, such as axonal damage, oligodendrocyte cell death, demyelination, autoimmunity, and blood-brain barrier dysfunction. Understanding of the mechanisms underlying glutamate toxicity in multiple sclerosis could help in the development of new approaches for diagnosis, treatment, and follow-up in patients with this debilitating disease. While several clinical trials of glutamatergic modulators have had disappointing results, our growing understanding suggests that there is reason to remain optimistic about the therapeutic potential of these drugs.

Overview

Integrity signals

Registry

Crossref · 10.1016/s1474-4422(16)30165-x

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Research works printed but not linked: 124

  1. Ernstsson, 2016, Cost of illness of multiple sclerosis—a systematic review, Plos One, 11, e0159129, 10.1371/journal.pone.0159129 · DOI
  2. Stys, 2013, Pathoetiology of multiple sclerosis: are we barking up the wrong tree?, F1000Prime Rep, 5, 20, 10.12703/P5-20 · DOI
  3. Collard, 2002, Neutrophil-derived glutamate regulates vascular endothelial barrier function, J Biol Chem, 277, 14801, 10.1074/jbc.M110557200 · DOI
  4. Pampliega, 2011, Increased expression of cystine/glutamate antiporter in multiple sclerosis, J Neuroinflammation, 8, 63, 10.1186/1742-2094-8-63 · DOI
  5. Evonuk, 2015, Inhibition of system Xc– transporter attenuates autoimmune inflammatory demyelination, J Immunol, 195, 450, 10.4049/jimmunol.1401108 · DOI
  6. Pacheco, 2006, Glutamate released by dendritic cells as a novel modulator of T cell activation, J Immunol, 177, 6695, 10.4049/jimmunol.177.10.6695 · DOI
  7. Domercq, 2005, Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition, Glia, 52, 36, 10.1002/glia.20221 · DOI
  8. Riedhammer, 2015, Antigen presentation, autoantigens, and immune regulation in multiple sclerosis and other autoimmune diseases, Front Immunol, 6, 322, 10.3389/fimmu.2015.00322 · DOI
  9. Waxman, 2006, Axonal conduction and injury in multiple sclerosis: the role of sodium channels, Nat Rev Neurosci, 7, 932, 10.1038/nrn2023 · DOI
  10. Affaticati, 2011, Sustained calcium signalling and caspase-3 activation involve NMDA receptors in thymocytes in contact with dendritic cells, Cell Death Differ, 18, 99, 10.1038/cdd.2010.79 · DOI
  11. Stys, 1993, Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons, PNAS, 90, 6976, 10.1073/pnas.90.15.6976 · DOI
  12. Dutta, 2006, Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients, Ann Neurol, 59, 478, 10.1002/ana.20736 · DOI
  13. Young, 2008, Imaging correlates of decreased axonal Na+/K+ ATPase in chronic multiple sclerosis lesions, Ann Neurol, 63, 428, 10.1002/ana.21381 · DOI
  14. Chen, 2015, Tumor necrosis factor-α enhances voltage-gated Na+ currents in primary culture of mouse cortical neurons, J Neuroinflammation, 12, 126, 10.1186/s12974-015-0349-x · DOI
  15. Shen, 2013, Interleukin-10 down-regulates voltage gated sodium channels in rat dorsal root ganglion neurons, Exp Neurol, 247, 466, 10.1016/j.expneurol.2013.01.018 · DOI
  16. Craner, 2004, Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger, Proc Natl Acad Sci, 101, 8168, 10.1073/pnas.0402765101 · DOI
  17. Bouafia, 2014, Axonal expression of sodium channels and neuropathology of the plaques in multiple sclerosis, Neuropathol Appl Neurobiol, 40, 579, 10.1111/nan.12059 · DOI
  18. Inglese, 2010, Brain tissue sodium concentration in multiple sclerosis: a sodium imaging study at 3 tesla, Brain, 133, 847, 10.1093/brain/awp334 · DOI
  19. Waxman, 2008, Mechanisms of disease: sodium channels and neuroprotection in multiple sclerosis—current status, Nat Clin Pract Neurol, 4, 159, 10.1038/ncpneuro0735 · DOI
  20. Yang, 2015, Sodium channel blockers for neuroprotection in multiple sclerosis, Cochrane Database Syst Rev, 10, 10.1002/14651858.CD010422.pub2 · DOI
  21. Werner, 2001, Multiple sclerosis: altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage, Ann Neurol, 50, 169, 10.1002/ana.1077 · DOI
  22. Pitt, 2003, Glutamate uptake by oligodendrocytes: Implications for excitotoxicity in multiple sclerosis, Neurology, 61, 1113, 10.1212/01.WNL.0000090564.88719.37 · DOI
  23. Ohgoh, 2002, Altered expression of glutamate transporters in experimental autoimmune encephalomyelitis, J Neuroimmunol, 125, 170, 10.1016/S0165-5728(02)00029-2 · DOI
  24. Loría, 2010, An endocannabinoid tone limits excitotoxicity in vitro and in a model of multiple sclerosis, Neurobiol Dis, 37, 166, 10.1016/j.nbd.2009.09.020 · DOI
  25. Mandolesi, 2013, Interleukin-1β alters glutamate transmission at purkinje cell synapses in a mouse model of multiple sclerosis, J Neurosci, 33, 12105, 10.1523/JNEUROSCI.5369-12.2013 · DOI
  26. Vercellino, 2007, Altered glutamate reuptake in relapsing-remitting and secondary progressive multiple sclerosis cortex: correlation with microglia infiltration, demyelination, and neuronal and synaptic damage, J Neuropathol Exp Neurol, 66, 732, 10.1097/nen.0b013e31812571b0 · DOI · Paper page
  27. Marte, 2010, Alterations of glutamate release in the spinal cord of mice with experimental autoimmune encephalomyelitis, J Neurochem, 115, 343, 10.1111/j.1471-4159.2010.06923.x · DOI
  28. Trkov, 2012, Fingolimod—a sphingosine-like molecule inhibits vesicle mobility and secretion in astrocytes, Glia, 60, 1406, 10.1002/glia.22361 · DOI
  29. Thomas, 2014, Small molecule glutaminase inhibitors block glutamate release from stimulated microglia, Biochem Biophys Res Commun, 443, 32, 10.1016/j.bbrc.2013.11.043 · DOI
  30. Castegna, 2011, Oxidative stress and reduced glutamine synthetase activity in the absence of inflammation in the cortex of mice with experimental allergic encephalomyelitis, Neuroscience, 185, 97, 10.1016/j.neuroscience.2011.04.041 · DOI
  31. Bolton, 1997, MK-801 limits neurovascular dysfunction during experimental allergic encephalomyelitis, J Pharmacol Exp Ther, 282, 397, 10.1016/S0022-3565(24)36794-1 · DOI
  32. Pitt, 2000, Glutamate excitotoxicity in a model of multiple sclerosis, Nat Med, 6, 67, 10.1038/71555 · DOI · Paper page
  33. Smith, 2000, Autoimmune encephalomyelitis ameliorated by AMPA antagonists, Nat Med, 6, 62, 10.1038/71548 · DOI
  34. Paul, 2002, Modulation of blood-brain barrier dysfunction and neurological deficits during acute experimental allergic encephalomyelitis by the N-methyl-D-aspartate receptor antagonist memantine, J Pharmacol Exp Ther, 302, 50, 10.1124/jpet.302.1.50 · DOI
  35. Gilgun-Sherki, 2003, Riluzole suppresses experimental autoimmune encephalomyelitis: implications for the treatment of multiple sclerosis, Brain Res, 7, 196, 10.1016/S0006-8993(03)03343-2 · DOI
  36. Kanwar, 2004, Simultaneous neuroprotection and blockade of inflammation reverses autoimmune encephalomyelitis, Brain, 127, 1313, 10.1093/brain/awh156 · DOI
  37. Docagne, 2007, Excitotoxicity in a chronic model of multiple sclerosis: neuroprotective effects of cannabinoids through CB1 and CB2 receptor activation, Mol Cell Neurosci, 34, 551, 10.1016/j.mcn.2006.12.005 · DOI
  38. Sulkowski, 2013, Effects of antagonists of glutamate receptors on pro-inflammatory cytokines in the brain cortex of rats subjected to experimental autoimmune encephalomyelitis, J Neuroimmunol, 261, 67, 10.1016/j.jneuroim.2013.05.006 · DOI
  39. Zhai, 2015, Blocking GluR2-GAPDH ameliorates experimental autoimmune encephalomyelitis, Ann Clin Transl Neurol, 2, 388, 10.1002/acn3.182 · DOI
  40. Pitt, 2000, Glutamate excitotoxicity in a model of multiple sclerosis, Nat Med, 6, 67, 10.1038/71555 · DOI · Paper page
  41. Ouardouz, 2009, Glutamate receptors on myelinated spinal cord axons: II. AMPA and GluR5 receptors, Ann Neurol, 65, 160, 10.1002/ana.21539 · DOI
  42. Stirling, 2010, Mechanisms of axonal injury: internodal nanocomplexes and calcium deregulation, Trends Mol Med, 16, 160, 10.1016/j.molmed.2010.02.002 · DOI
  43. McCarran, 2007, White matter axon vulnerability to AMPA/kainate receptor-mediated ischemic injury is developmentally regulated, J Neurosci, 27, 4220, 10.1523/JNEUROSCI.5542-06.2007 · DOI
  44. Cuthill, 2006, Different patterns of axonal damage after intracerebral injection of malonate or AMPA, Exp Neurol, 200, 509, 10.1016/j.expneurol.2006.03.021 · DOI
  45. Joshi, 2015, AMPA receptor activation causes preferential mitochondrial Ca2+ load and oxidative stress in motor neurons, Brain Res, 1616, 1, 10.1016/j.brainres.2015.04.042 · DOI
  46. Carriedo, 2000, AMPA exposures induce mitochondrial Ca2+ overload and ROS generation in spinal motor neurons in vitro, J Neurosci, 20, 240, 10.1523/JNEUROSCI.20-01-00240.2000 · DOI
  47. Williams, 2013, Mitochondrial calcium uptake, Proc Natl Acad Sci USA, 110, 10479, 10.1073/pnas.1300410110 · DOI
  48. Mahad, 2008, Review: mitochondria and disease progression in multiple sclerosis, Neuropathol Appl Neurobiol, 34, 577, 10.1111/j.1365-2990.2008.00987.x · DOI · Paper page
  49. Witte, 2009, Enhanced number and activity of mitochondria in multiple sclerosis lesions, J Pathol, 219, 193, 10.1002/path.2582 · DOI
  50. Broadwater, 2011, Analysis of the mitochondrial proteome in multiple sclerosis cortex, Biochim Biophys Acta, 1812, 630, 10.1016/j.bbadis.2011.01.012 · DOI
  51. Trapp, 2009, Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis, Lancet Neurol, 8, 280, 10.1016/S1474-4422(09)70043-2 · DOI · Paper page
  52. Centonze, 2009, Inflammation triggers synaptic alteration and degeneration in experimental autoimmune encephalomyelitis, J Neurosci, 29, 3442, 10.1523/JNEUROSCI.5804-08.2009 · DOI · Paper page
  53. Wallström, 1996, Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis, J Neurol Sci, 137, 89, 10.1016/0022-510X(95)00339-4 · DOI
  54. Okamoto, 2009, Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin, Nat Med, 15, 1407, 10.1038/nm.2056 · DOI
  55. Ksiazek-Winiarek, 2015, Neural plasticity in multiple sclerosis: the functional and molecular background, Neural Plast, 2015, 307175, 10.1155/2015/307175 · DOI
  56. Rossi, 2013, Opposite roles of NMDA receptors in relapsing and primary progressive multiple sclerosis, PLoS ONE, 8, e67357, 10.1371/journal.pone.0067357 · DOI
  57. Rossi, 2012, Interleukin-1β causes synaptic hyperexcitability in multiple sclerosis, Ann Neurol, 71, 76, 10.1002/ana.22512 · DOI
  58. Geurts, 2008, Grey matter pathology in multiple sclerosis, Lancet Neurol, 7, 841, 10.1016/S1474-4422(08)70191-1 · DOI
  59. Dutta, 2011, Demyelination causes synaptic alterations in hippocampi from multiple sclerosis patients, Ann Neurol, 69, 445, 10.1002/ana.22337 · DOI
  60. Matute, 2011, Glutamate and ATP signalling in white matter pathology, J Anat, 219, 53, 10.1111/j.1469-7580.2010.01339.x · DOI
  61. Hamilton, 2016, Proton-gated Ca2+-permeable TRP channels damage myelin in conditions mimicking ischaemia, Nature, 529, 523, 10.1038/nature16519 · DOI
  62. Matute, 2007, P2X7 receptor blockade prevents ATP excitotoxicity in oligodendrocytes and ameliorates experimental autoimmune encephalomyelitis, J Neurosci, 27, 9525, 10.1523/JNEUROSCI.0579-07.2007 · DOI
  63. Salter, 2005, NMDA receptors are expressed in developing oligodendrocyte processes and mediate injury, Nature, 438, 1167, 10.1038/nature04301 · DOI
  64. Micu, 2006, NMDA receptors mediate calcium accumulation in myelin during chemical ischaemia, Nature, 439, 988, 10.1038/nature04474 · DOI
  65. Piña-Crespo, 2010, Excitatory glycine responses of CNS myelin mediated by NR1/NR3 ‘NMDA’ receptor subunits, J Neurosci, 30, 11501, 10.1523/JNEUROSCI.1593-10.2010 · DOI
  66. Newcombe, 2008, Glutamate receptor expression in multiple sclerosis lesions, Brain Pathol, 18, 52, 10.1111/j.1750-3639.2007.00101.x · DOI
  67. Alberdi, 2002, Ca2+ influx through AMPA or kainate receptors alone is sufficient to initiate excitotoxicity in cultured oligodendrocytes, Neurobiol Dis, 9, 234, 10.1006/nbdi.2001.0457 · DOI
  68. Mato, 2013, Cytosolic zinc accumulation contributes to excitotoxic oligodendroglial death, Glia, 61, 750, 10.1002/glia.22470 · DOI
  69. Domercq, 2013, Zn2+-induced ERK activation mediates PARP-1-dependent ischemic-reoxygenation damage to oligodendrocytes, Glia, 61, 383, 10.1002/glia.22441 · DOI
  70. Bossy-Wetzel, 2004, Crosstalk between nitric oxide and zinc pathways to neuronal cell death involving mitochondrial dysfunction and p38-activated K+ channels, Neuron, 41, 351, 10.1016/S0896-6273(04)00015-7 · DOI
  71. Domercq, 2011, Dual-specific phosphatase-6 (Dusp6) and ERK mediate AMPA receptor-induced oligodendrocyte death, J Biol Chem, 286, 11825, 10.1074/jbc.M110.153049 · DOI
  72. Bannerman, 2007, GluR2-free alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors intensify demyelination in experimental autoimmune encephalomyelitis, J Neurochem, 102, 1064, 10.1111/j.1471-4159.2007.04612.x · DOI
  73. Ganor, 2003, Human T cells express a functional ionotropic glutamate receptor GluR3, and glutamate by itself triggers integrin-mediated adhesion to laminin and fibronectin and chemotactic migration, J Immunol, 170, 4362, 10.4049/jimmunol.170.8.4362 · DOI
  74. Sarchielli, 2007, Expression of ionotropic glutamate receptor GLUR3 and effects of glutamate on MBP- and MOG-specific lymphocyte activation and chemotactic migration in multiple sclerosis patients, J Neuroimmunol, 188, 146, 10.1016/j.jneuroim.2007.05.021 · DOI
  75. Lombardi, 2001, Characterization of ionotropic glutamate receptors in human lymphocytes, Br J Pharmacol, 133, 936, 10.1038/sj.bjp.0704134 · DOI
  76. Mashkina, 2010, NMDA receptors are expressed in lymphocytes activated both in vitro and in vivo, Cell Mol Neurobiol, 30, 901, 10.1007/s10571-010-9519-7 · DOI
  77. Boldyrev, 2004, Rodent lymphocytes express functionally active glutamate receptors, Biochem Biophys Res Commun, 324, 133, 10.1016/j.bbrc.2004.09.019 · DOI
  78. Lindblad, 2012, The N-methyl-d-aspartic acid receptor antagonist memantine ameliorates and delays the development of arthritis by enhancing regulatory T cells, Neurosignals, 20, 61, 10.1159/000329551 · DOI
  79. Reijerkerk, 2010, The NR1 subunit of NMDA receptor regulates monocyte transmigration through the brain endothelial cell barrier, J Neurochem, 113, 447, 10.1111/j.1471-4159.2010.06598.x · DOI
  80. András, 2007, The NMDA and AMPA/KA receptors are involved in glutamate-induced alterations of occludin expression and phosphorylation in brain endothelial cells, J Cereb Blood Flow Metab, 27, 1431, 10.1038/sj.jcbfm.9600445 · DOI
  81. Kamat, 2015, Hydrogen sulfide epigenetically attenuates homocysteine-induced mitochondrial toxicity mediated through NMDA receptor in mouse brain endothelial (bEnd3) cells, J Cell Physiol, 230, 378, 10.1002/jcp.24722 · DOI
  82. Sharp, 2003, Glutamate causes a loss in human cerebral endothelial barrier integrity through activation of NMDA receptor, Am J Physiol Heart Circ Physiol, 285, H2592, 10.1152/ajpheart.00520.2003 · DOI
  83. Scott, 2007, Glutamate-stimulated peroxynitrite production in a brain-derived endothelial cell line is dependent on N-methyl-D-aspartate (NMDA) receptor activation, Biochem Pharmacol, 73, 228, 10.1016/j.bcp.2006.09.021 · DOI
  84. Bolton, 2006, Glutamate receptors in neuroinflammatory demyelinating disease, Mediators Inflamm, 2006, 93684, 10.1155/MI/2006/93684 · DOI
  85. Basuroy, 2006, MAPK interacts with occludin and mediates EGF-induced prevention of tight junction disruption by hydrogen peroxide, Biochem J, 393, 69, 10.1042/BJ20050959 · DOI
  86. Lipton, 1993, A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds, Nature, 364, 626, 10.1038/364626a0 · DOI · Paper page
  87. Nakamura, 2013, Aberrant protein s-nitrosylation in neurodegenerative diseases, Neuron, 78, 596, 10.1016/j.neuron.2013.05.005 · DOI
  88. Sarchielli, 2003, Excitatory amino acids and multiple sclerosis: evidence from cerebrospinal fluid, Arch Neurol, 60, 1082, 10.1001/archneur.60.8.1082 · DOI · Paper page
  89. Srinivasan, 2005, Evidence of elevated glutamate in multiple sclerosis using magnetic resonance spectroscopy at 3 T, Brain, 128, 1016, 10.1093/brain/awh467 · DOI
  90. Baranzini, 2010, Genetic variation influences glutamate concentrations in brains of patients with multiple sclerosis, Brain, 133, 2603, 10.1093/brain/awq192 · DOI
  91. Tisell, 2013, Increased concentrations of glutamate and glutamine in normal-appearing white matter of patients with multiple sclerosis and normal MR imaging brain scans, PLoS One, 8, e61817, 10.1371/journal.pone.0061817 · DOI
  92. Azevedo, 2014, In vivo evidence of glutamate toxicity in multiple sclerosis, Ann Neurol, 76, 269, 10.1002/ana.24202 · DOI · Paper page
  93. Muhlert, 2014, Memory in multiple sclerosis is linked to glutamate concentration in grey matter regions, J Neurol Neurosurg Psychiatr, 85, 833, 10.1136/jnnp-2013-306662 · DOI
  94. Urenjak, 1992, Specific expression of N-acetylaspartate in neurons, oligodendrocyte-type-2 astrocyte progenitors, and immature oligodendrocytes in vitro, J Neurochem, 59, 55, 10.1111/j.1471-4159.1992.tb08875.x · DOI
  95. Narayana, 2005, Magnetic resonance spectroscopy in the monitoring of multiple sclerosis, J Neuroimaging, 15, 46S, 10.1177/1051228405284200 · DOI
  96. Marliani, 2010, Quantitative cervical spinal cord 3T proton MR spectroscopy in multiple sclerosis, AJNR Am J Neuroradiol, 31, 180, 10.3174/ajnr.A1738 · DOI
  97. Kogan, 2013, Imaging of glutamate in the spinal cord using GluCEST, Neuroimage, 77, 262, 10.1016/j.neuroimage.2013.03.072 · DOI
  98. Abdel-Aziz, 2014, Age related changes in metabolite concentrations in the normal spinal cord, PLoS One, 9, e105774, 10.1371/journal.pone.0105774 · DOI
  99. Pampliega, 2008, Association of an EAAT2 polymorphism with higher glutamate concentration in relapsing multiple sclerosis, J Neuroimmunol, 195, 194, 10.1016/j.jneuroim.2008.01.011 · DOI
  100. Strijbis, 2013, Glutamate gene polymorphisms predict brain volumes in multiple sclerosis, Mult Scler, 19, 281, 10.1177/1352458512454345 · DOI
  101. Comabella, 2009, Genome-wide scan of 500,000 single-nucleotide polymorphisms among responders and nonresponders to interferon beta therapy in multiple sclerosis, Arch Neurol, 66, 972, 10.1001/archneurol.2009.150 · DOI
  102. Kostic, 2014, IL-17 and glutamate excitotoxicity in the pathogenesis of multiple sclerosis, Scand J Immunol, 79, 181, 10.1111/sji.12147 · DOI
  103. Eisenstein, 2009, The T(reg)/Th17 cell balance: a new paradigm for autoimmunity, Pediatr Res, 65, 26R, 10.1203/PDR.0b013e31819e76c7 · DOI
  104. MacDonald, 2006, Paradox of Ca2+ signaling, cell death and stroke, Trends Neurosci, 29, 75, 10.1016/j.tins.2005.12.001 · DOI
  105. Krupp, 1995, Fatigue therapy in multiple sclerosis: results of a double-blind, randomized, parallel trial of amantadine, pemoline, and placebo, Neurology, 45, 1956, 10.1212/WNL.45.11.1956 · DOI
  106. Villoslada, 2009, Memantine induces reversible neurologic impairment in patients with MS, Neurology, 72, 1630, 10.1212/01.wnl.0000342388.73185.80 · DOI
  107. Lovera, 2010, Memantine for cognitive impairment in multiple sclerosis: a randomized placebo-controlled trial, Mult Scler, 16, 715, 10.1177/1352458510367662 · DOI
  108. Thurtell, 2010, Crossover trial of gabapentin and memantine as treatment for acquired nystagmus, Ann Neurol, 67, 676, 10.1002/ana.21991 · DOI
  109. Mehta, 2010, A randomized trial of memantine as treatment for spasticity in multiple sclerosis, Mult Scler, 16, 248, 10.1177/1352458509355462 · DOI
  110. Waubant, 2014, A randomized controlled phase II trial of riluzole in early multiple sclerosis, Ann Clin Transl Neurol, 1, 340, 10.1002/acn3.60 · DOI
  111. Peyro Saint Paul, 2016, Efficacy and safety profile of memantine in patients with cognitive impairment in multiple scelrosis, J Neurol Sci, 363, 69, 10.1016/j.jns.2016.02.012 · DOI
  112. Kornhuber, 1991, Effects of the 1-amino-adamantanes at the MK-801-binding site of the NMDA-receptor-gated ion channel: a human postmortem brain study, Eur J Pharmacol, 206, 297, 10.1016/0922-4106(91)90113-V · DOI
  113. Blanchet, 2003, Renaissance of amantadine in the treatment of Parkinson's disease, Adv Neurol, 91, 251
  114. Pucci, 2007, Amantadine for fatigue in multiple sclerosis, Cochrane Database Syst Rev, 1, 10.1002/14651858.CD002818.pub2 · DOI
  115. Lipton, 2006, Paradigm shift in neuroprotection by NMDA receptor blockade: memantine and beyond, Nat Rev Drug Discov, 5, 160, 10.1038/nrd1958 · DOI · Paper page
  116. Lipton, 2007, Pathologically activated therapeutics for neuroprotection, Nat Rev Neurosci, 8, 803, 10.1038/nrn2229 · DOI
  117. Killestein, 2005, Glutamate inhibition in MS: the neuroprotective properties of riluzole, J Neurol Sci, 233, 113, 10.1016/j.jns.2005.03.011 · DOI
  118. Kalkers, 2002, The effect of the neuroprotective agent riluzole on MRI parameters in primary progressive multiple sclerosis: a pilot study, Mult Scler, 8, 532, 10.1191/1352458502ms849xx · DOI
  119. Lipton, 2006, NMDA receptors, glial cells, and clinical medicine, Neuron, 50, 9, 10.1016/j.neuron.2006.03.026 · DOI
  120. Stys, 2007, White matter NMDA receptors: an unexpected new therapeutic target?, Trends Pharmacol Sci, 28, 561, 10.1016/j.tips.2007.10.003 · DOI
  121. LeMaistre, 2012, Coactivation of NMDA receptors by glutamate and D-serine induces dilation of isolated middle cerebral arteries, J Cereb Blood Flow Metab, 32, 537, 10.1038/jcbfm.2011.161 · DOI
  122. Russo, 2012, New AMPA antagonists in epilepsy, Expert Opin Investig Drugs, 21, 1371, 10.1517/13543784.2012.705277 · DOI
  123. Krauss, 2013, Perampanel: a selective AMPA antagonist for treating seizures, Epilepsy Curr, 13, 269, 10.5698/1535-7597-13.6.269 · DOI
  124. Macrez R, Ortega MC, Bardou I, et al. Neuroendothelial NMDA receptors as therapeutic targets in experimental autoimmune encephalomyelitis. Brain (in press). · DOI

Cited by

Sorted by citations

See all 127

Metadata

Authors
Macrez, R., Stys, P. K., Vivien, D., Lipton, S. A., & Docagne, F.
Venue
The Lancet Neurology
Publisher
Elsevier BV
Published
2016-09
Volume
15
Issue
10
Pages
1089-1102
ISSN
1474-4422
DOI
10.1016/s1474-4422(16)30165-x
Cited by
127
References
5
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review