Alternation of neurofilaments in immune-mediated injury of spinal cord motor neurons

[1]  M. Strong,et al.  The Pathobiology of Amyotrophic Lateral Sclerosis: A Proteinopathy? , 2005, Journal of neuropathology and experimental neurology.

[2]  P. Shaw,et al.  Molecular and cellular pathways of neurodegeneration in motor neurone disease , 2005, Journal of Neurology, Neurosurgery & Psychiatry.

[3]  C. Shaw,et al.  Neurofilament heavy chain side arm phosphorylation regulates axonal transport of neurofilaments , 2003, The Journal of cell biology.

[4]  B. Liu,et al.  Role of Nitric Oxide in Inflammation‐Mediated Neurodegeneration , 2002, Annals of the New York Academy of Sciences.

[5]  S Cluskey,et al.  Mechanisms of neurodegeneration in amyotrophic lateral sclerosis , 2001, Molecular pathology : MP.

[6]  H. Pant,et al.  Cyclin-dependent protein kinase 5 (Cdk5) and the regulation of neurofilament metabolism. , 2001, European journal of biochemistry.

[7]  T. Gotow,et al.  Neurofilaments in health and disease , 2000, Medical Electron Microscopy.

[8]  C. Geula,et al.  Motor neurons are rich in non-phosphorylated neurofilaments: cross-species comparison and alterations in ALS , 2000, Brain Research.

[9]  M. Strong Neurofilament metabolism in sporadic amyotrophic lateral sclerosis , 1999, Journal of the Neurological Sciences.

[10]  Jean-Pierre Julien,et al.  Neurofilament functions in health and disease , 1999, Current Opinion in Neurobiology.

[11]  P. Leigh,et al.  Cyclin dependent kinase-5 (CDK-5) phosphorylates neurofilament heavy (NF-H) chain to generate epitopes for antibodies that label neurofilament accumulations in amyotrophic lateral sclerosis (ALS) and is present in affected motor neurones in ALS , 1999, Progress in Neuro-Psychopharmacology and Biological Psychiatry.

[12]  Guy A. Rouleau,et al.  SOD1 mutation is assosiated with accumulation of neurofilaments in amyotrophic lateral scelaries , 1996 .

[13]  A. Clark,et al.  SOD1 mutation is associated with accumulation of neurofilaments in amyotrophic lateral sclerosis. , 1996, Annals of neurology.

[14]  S. Brady Mice overexpressing the human neurofilament heavy gene as a model of ALS , 1995, Neurobiology of Aging.

[15]  E. Stefani,et al.  Amyotrophic lateral sclerosis patient antibodies label Ca2+ channel α1 subunit , 1994 .

[16]  E. Stefani,et al.  Amyotrophic lateral sclerosis patient antibodies label Ca2+ channel alpha 1 subunit. , 1994, Annals of neurology.

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

[18]  E. Stefani,et al.  Serum antibodies to L-type calcium channels in patients with amyotrophic lateral sclerosis. , 1992, The New England journal of medicine.

[19]  S. Appel,et al.  IgG reactivity in the spinal cord and motor cortex in amyotrophic lateral sclerosis. , 1990, Archives of neurology.

[20]  S. Appel,et al.  Motor neuron destruction in guinea pigs immunized with bovine spinal cord ventral horn homogenate: experimental autoimmune gray matter disease , 1990, Journal of Neuroimmunology.

[21]  S. Appel,et al.  Experimental autoimmune motoneuron disease , 1989, Annals of neurology.

[22]  S. Appel,et al.  Amyotrophic lateral sclerosis. Associated clinical disorders and immunological evaluations. , 1986, Archives of Neurology.