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Asao Hirano – One of the best experts on this subject based on the ideXlab platform.

  • differential expression between synaptic vesicle proteins and presynaptic plasma membrane proteins in the Anterior Horn of amyotrophic lateral sclerosis
    Acta Neuropathologica, 2002
    Co-Authors: Akito Ikemoto, I Akiguchi, Shinichi Nakamura, Asao Hirano

    Abstract:

    This study concerns the immunohistochemical investigation of synaptic proteins in the Anterior Horn of amyotrophic lateral sclerosis (ALS). Antibodies against synapsin 1 and synaptophysin (i.e. synaptic vesicle proteins), and those against syntaxin and the synaptosomal-associated, 25 kDa protein, SNAP25 (i.e. presynaptic plasma membrane proteins) were used for immunostaining, respectively. Lumbar spinal cords from five ALS and eight control patients were examined. In the controls, all four synaptic proteins exhibited fine granular immunoreactivities, distributed throughout the spinal gray matter almost uniformly. In contrast, in all five ALS patients, two of the synaptic vesicle proteins examined decreased in the Anterior Horn neuropil diffusely, while in the same lumbar segments of these cases the immunoreactivities of the two presynaptic plasma membrane proteins showed no apparent decrease, or were only mildly diminished in the same gray matter area. These results indicate that, during the presynaptic terminal degeneration in the Anterior Horn of ALS, synaptic vesicle involvement may precede that of the presynaptic plasma membrane.

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  • Increased expression of growth-associated protein 43 on the surface of the Anterior Horn cells in amyotrophic lateral sclerosis.
    Acta Neuropathologica, 1999
    Co-Authors: Akito Ikemoto, Asao Hirano, I Akiguchi

    Abstract:

    This study examined axonal terminal alterations in the Anterior Horn of amyotrophic lateral sclerosis (ALS) patients. An antibody against growth-associated protein 43 (GAP43), a phosphoprotein which is expressed in elongating terminals of neurites, was employed for immunohistochemical staining. Lumbar spinal cords taken at autopsy from five ALS patients and from six control adults were examined. In control patients, there were numerous GAP43-positive granules diffusely dispersed throughout the Anterior Horn neuropil, and individual large Anterior Horn cells (AHCs) showed numerous tiny immunoreactive granules and small dots on the surface. A small number of AHCs showed dense accumulation of GAP43 immunoreactivity on the surface of the cell body and proximal processes. In all ALS patients, similar accumulation of GAP43 immunoreactivity was seen on the surface of a large number of remaining AHCs. Statistical analysis revealed a significant increase in number of AHCs with such accumulation in ALS patients. These results suggest that during the ALS disease process there may be plastic alterations or a compensatory mechanism of the axonal terminals located on the surface of some AHCs for ongoing Anterior Horn presynaptic terminal degeneration.

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  • Comparative immunohistochemical study on synaptophysin expression in the Anterior Horn of post-poliomyelitis and sporadic amyotrophic lateral sclerosis.
    Acta Neuropathologica, 1996
    Co-Authors: Akito Ikemoto, Asao Hirano

    Abstract:

    This report concerns a comparative study of alterations of Anterior Horn presynaptic terminals in post-poliomyelitis and sporadic amyotrophic lateral sclerosis (S-ALS). Synaptophysin (SP) served as a marker for presynaptic terminals; immunohistochemical techniques were used throughout. Spinal cords from six individuals without neurological disease served as controls. Localized and well-delineated Anterior Horn neuropil areas with decreased SP immunoreactivity were observed in the five cases of post-poliomyelitis studied. These areas had few remaining neurons but had pronounced reactive gliosis which corresponded to those areas in which typical poliomyelitis lesions were present. Normal neuronal SP expression was preserved in the adjacent, non-affected areas. However, a small region with increased SP levels was observed in one case. By comparison, the decrease in Anterior Horn SP immunoreactivity was diffuse in the four S-ALS patients studied. The present data suggest that presynaptic terminals ending at the somata and processes of affected Anterior Horn neurons located in the area of the acute infection are degenerate in post-poliomyelitis. By contrast, in S-ALS the terminals ending at distal dendrite portions tend to be severely degenerate, while those terminating at the proximal portions of the neuron are relatively well preserved. Our results thus provide additional evidence that the pathogenesis of the post-poliomyelitis state differs from that of ALS.

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Michael Swash – One of the best experts on this subject based on the ideXlab platform.

  • fasciculation cramp syndrome preceding Anterior Horn cell disease an intermediate syndrome
    Journal of Neurology Neurosurgery and Psychiatry, 2011
    Co-Authors: Mamede De Carvalho, Michael Swash

    Abstract:

    Cramp-fasciculation syndrome (cramp-FS) is an ill-defined condition with uncertain clinical limits. The authors studied a 55-year-old man with progressively more severe, widespread fasciculations and cramps during a 6-year-period. Mild progressive lower motor neuron loss, shown by motor unit number and multi-motor unit potential (MUP) analysis, developed during the 4 years after onset, which stabilised during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of Anterior Horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.

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  • Fasciculation-cramp syndrome preceding Anterior Horn cell disease: an intermediate syndrome?
    Journal of Neurology Neurosurgery and Psychiatry, 2010
    Co-Authors: Mamede De Carvalho, Michael Swash

    Abstract:

    Cramp-fasciculation syndrome (cramp-FS) is an ill-defined condition with uncertain clinical limits. We studied a 55-year-old man with progressively more severe, widespread fasciculations and cramps during a six-year period. Mild progressive lower motor neuron loss, shown by MUNE and multiMUP analysis, developed during the four years after onset, which stabilized during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of Anterior Horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.

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Akito Ikemoto – One of the best experts on this subject based on the ideXlab platform.

  • differential expression between synaptic vesicle proteins and presynaptic plasma membrane proteins in the Anterior Horn of amyotrophic lateral sclerosis
    Acta Neuropathologica, 2002
    Co-Authors: Akito Ikemoto, I Akiguchi, Shinichi Nakamura, Asao Hirano

    Abstract:

    This study concerns the immunohistochemical investigation of synaptic proteins in the Anterior Horn of amyotrophic lateral sclerosis (ALS). Antibodies against synapsin 1 and synaptophysin (i.e. synaptic vesicle proteins), and those against syntaxin and the synaptosomal-associated, 25 kDa protein, SNAP25 (i.e. presynaptic plasma membrane proteins) were used for immunostaining, respectively. Lumbar spinal cords from five ALS and eight control patients were examined. In the controls, all four synaptic proteins exhibited fine granular immunoreactivities, distributed throughout the spinal gray matter almost uniformly. In contrast, in all five ALS patients, two of the synaptic vesicle proteins examined decreased in the Anterior Horn neuropil diffusely, while in the same lumbar segments of these cases the immunoreactivities of the two presynaptic plasma membrane proteins showed no apparent decrease, or were only mildly diminished in the same gray matter area. These results indicate that, during the presynaptic terminal degeneration in the Anterior Horn of ALS, synaptic vesicle involvement may precede that of the presynaptic plasma membrane.

    Free Register to Access Article

  • Increased expression of growth-associated protein 43 on the surface of the Anterior Horn cells in amyotrophic lateral sclerosis.
    Acta Neuropathologica, 1999
    Co-Authors: Akito Ikemoto, Asao Hirano, I Akiguchi

    Abstract:

    This study examined axonal terminal alterations in the Anterior Horn of amyotrophic lateral sclerosis (ALS) patients. An antibody against growth-associated protein 43 (GAP43), a phosphoprotein which is expressed in elongating terminals of neurites, was employed for immunohistochemical staining. Lumbar spinal cords taken at autopsy from five ALS patients and from six control adults were examined. In control patients, there were numerous GAP43-positive granules diffusely dispersed throughout the Anterior Horn neuropil, and individual large Anterior Horn cells (AHCs) showed numerous tiny immunoreactive granules and small dots on the surface. A small number of AHCs showed dense accumulation of GAP43 immunoreactivity on the surface of the cell body and proximal processes. In all ALS patients, similar accumulation of GAP43 immunoreactivity was seen on the surface of a large number of remaining AHCs. Statistical analysis revealed a significant increase in number of AHCs with such accumulation in ALS patients. These results suggest that during the ALS disease process there may be plastic alterations or a compensatory mechanism of the axonal terminals located on the surface of some AHCs for ongoing Anterior Horn presynaptic terminal degeneration.

    Free Register to Access Article

  • Comparative immunohistochemical study on synaptophysin expression in the Anterior Horn of post-poliomyelitis and sporadic amyotrophic lateral sclerosis.
    Acta Neuropathologica, 1996
    Co-Authors: Akito Ikemoto, Asao Hirano

    Abstract:

    This report concerns a comparative study of alterations of Anterior Horn presynaptic terminals in post-poliomyelitis and sporadic amyotrophic lateral sclerosis (S-ALS). Synaptophysin (SP) served as a marker for presynaptic terminals; immunohistochemical techniques were used throughout. Spinal cords from six individuals without neurological disease served as controls. Localized and well-delineated Anterior Horn neuropil areas with decreased SP immunoreactivity were observed in the five cases of post-poliomyelitis studied. These areas had few remaining neurons but had pronounced reactive gliosis which corresponded to those areas in which typical poliomyelitis lesions were present. Normal neuronal SP expression was preserved in the adjacent, non-affected areas. However, a small region with increased SP levels was observed in one case. By comparison, the decrease in Anterior Horn SP immunoreactivity was diffuse in the four S-ALS patients studied. The present data suggest that presynaptic terminals ending at the somata and processes of affected Anterior Horn neurons located in the area of the acute infection are degenerate in post-poliomyelitis. By contrast, in S-ALS the terminals ending at distal dendrite portions tend to be severely degenerate, while those terminating at the proximal portions of the neuron are relatively well preserved. Our results thus provide additional evidence that the pathogenesis of the post-poliomyelitis state differs from that of ALS.

    Free Register to Access Article