Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man
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J. Glass | J. Khan | M. Polak | A. Davis | A. Castellano-Sanchez | L. Fischer | D. Culver | P. Tennant | Minsheng Wang | J. Khan
[1] Paris Jean Aicardi,et al. Diseases of the Nervous System: Clinical Neuroscience and Therapeutic Principles , 2004, European Child & Adolescent Psychiatry.
[2] Yasushi Hiraoka,et al. Mutations in Dynein Link Motor Neuron Degeneration to Defects in Retrograde Transport , 2003, Science.
[3] J. Sanes,et al. Inhibiting Axon Degeneration and Synapse Loss Attenuates Apoptosis and Disease Progression in a Mouse Model of Motoneuron Disease , 2003, Current Biology.
[4] Shin J. Oh,et al. Mutant dynactin in motor neuron disease , 2003, Nature Genetics.
[5] Robert G. Miller,et al. Drug therapy for amyotrophic lateral sclerosis: Where are we now? , 2003, IDrugs : the investigational drugs journal.
[6] J. Rothstein,et al. Cyclooxygenase 2 inhibition protects motor neurons and prolongs survival in a transgenic mouse model of ALS , 2002, Annals of neurology.
[7] M. Pinter,et al. Reduced neuromuscular quantal content with normal synaptic release time course and depression in canine motor neuron disease. , 2002, Journal of neurophysiology.
[8] S. Wiese,et al. Missense mutation in the tubulin-specific chaperone E (Tbce) gene in the mouse mutant progressive motor neuronopathy, a model of human motoneuron disease , 2002, The Journal of cell biology.
[9] G. Mckhann,et al. Pathophysiology of nerve and root disorders , 2002 .
[10] E. Salido,et al. A missense mutation in Tbce causes progressive motor neuronopathy in mice , 2002, Nature Genetics.
[11] V. Perry,et al. Axon pathology in neurological disease: a neglected therapeutic target , 2002, Trends in Neurosciences.
[12] J. Melki,et al. Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse model. , 2002, Human molecular genetics.
[13] D. Howland,et al. Disruption of Dynein/Dynactin Inhibits Axonal Transport in Motor Neurons Causing Late-Onset Progressive Degeneration , 2002, Neuron.
[14] M. Gurney,et al. Formation of high molecular weight complexes of mutant Cu, Zn-superoxide dismutase in a mouse model for familial amyotrophic lateral sclerosis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[15] P. Caroni,et al. Early and Selective Loss of Neuromuscular Synapse Subtypes with Low Sprouting Competence in Motoneuron Diseases , 2000, The Journal of Neuroscience.
[16] M. Raff,et al. Evidence That Wallerian Degeneration and Localized Axon Degeneration Induced by Local Neurotrophin Deprivation Do Not Involve Caspases , 2000, The Journal of Neuroscience.
[17] D. Cleveland,et al. Slowing of axonal transport is a very early event in the toxicity of ALS–linked SOD1 mutants to motor neurons , 1999 .
[18] M. Gurney,et al. Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS , 1998 .
[19] M. Gurney,et al. Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS. , 1998, Glia.
[20] J. Trojanowski,et al. Neurofilaments and Orthograde Transport Are Reduced in Ventral Root Axons of Transgenic Mice that Express Human SOD1 with a G93A Mutation , 1997, The Journal of cell biology.
[21] R. Vejsada,et al. Clinical and molecular aspects of motoneurone diseases: animal models, neurotrophic factors and Bcl-2 oncoprotein. , 1997, Trends in pharmacological sciences.
[22] F. Finiels,et al. Neuromuscular function impairment is not caused by motor neurone loss in FALS mice: an electromyographic study. , 1996, Neuroreport.
[23] R. Coggeshall,et al. Methods for determining numbers of cells and synapses: A case for more uniform standards of review , 1996, The Journal of comparative neurology.
[24] J. Glass,et al. Immunocytochemical quantitation of human immunodeficiency virus in the brain: Correlations with dementia , 1995, Annals of neurology.
[25] M. Gurney,et al. Age-Dependent Penetrance of Disease in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis , 1995, Molecular and Cellular Neuroscience.
[26] T. Deckwerth,et al. Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis). , 1994, Developmental biology.
[27] 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.
[28] H. Gundersen,et al. Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator , 1991, The Anatomical record.
[29] M. Graeber,et al. Axotomy of the rat facial nerve leads to increased CR3 complement receptor expression by activated microglial cells , 1988, Journal of neuroscience research.
[30] J. Griffin,et al. Axonal transport in neurological disease , 1988, Annals of neurology.
[31] M. Graeber,et al. Reaction on Motoneurons and Their Microenvironment to Axotomy , 1986 .
[32] E. K. Bjornskov,et al. Quantitative axon terminal and end-plate morphology in amyotrophic lateral sclerosis. , 1984, Archives of neurology.
[33] W. Bradley,et al. Morphometric and biochemical studies of peripheral nerves in amyotrophic lateral sclerosis , 1983, Annals of neurology.
[34] G. Sobue,et al. Amyotrophic lateral sclerosis. Lack of central chromatolytic response of motor neurocytons corresponding to active axonal degeneration. , 1983, Archives of neurology.
[35] Cavanagh Jb. The significance of the "dying back" process in experimental and human neurological disease. , 1964 .