Anterior Horn

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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.

  • 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.

  • 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.

  • Synaptophysin expression in the Anterior Horn of Werdnig-Hoffmann disease.
    Journal of the Neurological Sciences, 1996
    Co-Authors: Akito Ikemoto, Asao Hirano, S Matsumoto, I Akiguchi, J Kimura
    Abstract:

    This report concerns the study of synaptophysin (SP) expression in the Anterior Horn in four cases of Werdnig-Hoffmann disease (WHD). All patients had distinct Anterior Horn cell degeneration, and died before the age of one year. Normal spinal cords from five age-matched children served as controls. Five cases of sporadic amyotrophic lateral sclerosis (S-ALS), three cases of lower motor neuron disease (L-MND), three cases of peripheral neuropathy with axonal reaction, and six adult cases with normal spinal cords were included for comparison. Immunohistochemical techniques were used throughout. The results show that normal spinal cords of children have similar SP immunoreactivity patterns as those of normal adults. We also found that despite relatively preserved or slightly increased SP immunoreactivity on the surface of the cell body and proximal processes of the remaining neurons, there was a diffuse decrease of immunoreaction product deposits in the Anterior Horn neuropil of the WHD cases. The ballooned neurons in the Anterior Horns of patients with WHD, S-ALS, L-MND, and axonal reaction had few SP immunoreactive dots or granules around the cell bodies and proximal processes. The perikarya of some ballooned neurons of the children with WHD was diffusely stained for SP. There was no SP immunoreactive structures within the empty cell beds of these patients. The observed decrease in SP expression around ballooned neurons in these disorders is indicative of a disconnection of presynaptic terminals of afferent fibers from the proximal portion of the swollen degenerated Anterior Horn cells.

  • Immunocytochemical studies on synaptophysin in the Anterior Horn of lower motor neuron disease.
    Journal of Neuropathology and Experimental Neurology, 1994
    Co-Authors: Akito Ikemoto, Toru Kawanami, Josefina F. Llena, Asao Hirano
    Abstract:

    This report concerns the study of synaptophysin (SP) expression in the Anterior Horn of three cases of lower motor neuron disease (L-MND). All patients studied had Anterior Horn cell degeneration without neuropathological evidence of corticospinal tract degeneration. Spinal cords from six patients with no neurological disease served as controls. Immunocytochemical techniques were used. The results show that in L-MND there is decreased SP immunoreactivity of the Anterior Horn neuropil, but preservation of immunoreactive dots around the cell body and proximal processes, and the presence of some residual neurons in the affected gray matter that are surrounded by a dense accumulation of immunoreaction products. These findings resemble those of classical amyotrophic lateral sclerosis (ALS), indicating similarities in the distribution patterns of presynaptic terminals in the Anterior Horn of L-MND and classical ALS.

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.

  • 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.

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.

  • 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.

  • 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.

  • Synaptophysin expression in the Anterior Horn of Werdnig-Hoffmann disease.
    Journal of the Neurological Sciences, 1996
    Co-Authors: Akito Ikemoto, Asao Hirano, S Matsumoto, I Akiguchi, J Kimura
    Abstract:

    This report concerns the study of synaptophysin (SP) expression in the Anterior Horn in four cases of Werdnig-Hoffmann disease (WHD). All patients had distinct Anterior Horn cell degeneration, and died before the age of one year. Normal spinal cords from five age-matched children served as controls. Five cases of sporadic amyotrophic lateral sclerosis (S-ALS), three cases of lower motor neuron disease (L-MND), three cases of peripheral neuropathy with axonal reaction, and six adult cases with normal spinal cords were included for comparison. Immunohistochemical techniques were used throughout. The results show that normal spinal cords of children have similar SP immunoreactivity patterns as those of normal adults. We also found that despite relatively preserved or slightly increased SP immunoreactivity on the surface of the cell body and proximal processes of the remaining neurons, there was a diffuse decrease of immunoreaction product deposits in the Anterior Horn neuropil of the WHD cases. The ballooned neurons in the Anterior Horns of patients with WHD, S-ALS, L-MND, and axonal reaction had few SP immunoreactive dots or granules around the cell bodies and proximal processes. The perikarya of some ballooned neurons of the children with WHD was diffusely stained for SP. There was no SP immunoreactive structures within the empty cell beds of these patients. The observed decrease in SP expression around ballooned neurons in these disorders is indicative of a disconnection of presynaptic terminals of afferent fibers from the proximal portion of the swollen degenerated Anterior Horn cells.

  • Immunocytochemical studies on synaptophysin in the Anterior Horn of lower motor neuron disease.
    Journal of Neuropathology and Experimental Neurology, 1994
    Co-Authors: Akito Ikemoto, Toru Kawanami, Josefina F. Llena, Asao Hirano
    Abstract:

    This report concerns the study of synaptophysin (SP) expression in the Anterior Horn of three cases of lower motor neuron disease (L-MND). All patients studied had Anterior Horn cell degeneration without neuropathological evidence of corticospinal tract degeneration. Spinal cords from six patients with no neurological disease served as controls. Immunocytochemical techniques were used. The results show that in L-MND there is decreased SP immunoreactivity of the Anterior Horn neuropil, but preservation of immunoreactive dots around the cell body and proximal processes, and the presence of some residual neurons in the affected gray matter that are surrounded by a dense accumulation of immunoreaction products. These findings resemble those of classical amyotrophic lateral sclerosis (ALS), indicating similarities in the distribution patterns of presynaptic terminals in the Anterior Horn of L-MND and classical ALS.

Shoichi Maruyama - One of the best experts on this subject based on the ideXlab platform.

  • Synapse loss in Anterior Horn neurons in amyotrophic lateral sclerosis
    Acta Neuropathologica, 1994
    Co-Authors: Shoichi Sasaki, Shoichi Maruyama
    Abstract:

    This report deals with an ultrastructural investigation of the synapses of Anterior Horn neurons in the lumbar spinal cords of five patients with amyotrophic lateral sclerosis (ALS) who had mild neuronal depletion. Specimens from five age-matched, neurologically normal individuals served as controls. In each instance, the autopsy was performed within 3 h after death. A statistically significant decrease in cell body area, number of synapses and total synaptic length was found in the normal-appearing neurons of the ALS patients. The alterations were more pronounced in neurons with central chromatolysis. However, despite an approximately 20% reduction in the number of synapses, the length of the active synaptic zone of the normal-appearing neurons in the ALS patients was not diminished. This observation may be accounted for by a plasticity to the loss of synapses which maintained the active zone of the remaining synapses to increase synaptic efficiency. It is suggested that when the plasticity of the active zone reaches its limit, the continuing loss of synapses may lead to functional impairment. The capacity of the active synaptic zone to respond to progressive denervation of the Anterior Horn neurons may preserve motor function or slow the development of motor deficits in the early stage of degeneration of the lower motor neurons.

  • ultrastructural study of bunina bodies in the Anterior Horn neurons of patients with amyotrophic lateral sclerosis
    Neuroscience Letters, 1993
    Co-Authors: Shoichi Sasaki, Shoichi Maruyama
    Abstract:

    Abstract We ultrastructurally investigated Bunina bodies (BB) in the Anterior Horn neurons of 20 amyotrophic lateral sclerosis patients with BB. As for novel findings, filaments thicker than neurofilaments were not uncommonly observed inside the BB. They were occasionally observed around the periphery of the BB. Some of them were composed of bundles of filaments which appeared constricted at 40–50 nm intervals and were 20–25 nm in maximum width. Others consisted of bundles of unconstricted filaments measuring about 20–25 nm in diameter. The BB occasionally contained bundles of filaments of about 20 nm in diameter that closely resembled those found in ubiquitin-positive skein-like inclusions. It seems that some molecular disturbances such as ubiquitin play a role in the formation of the constricted and unconstricted filaments. Probably cytoskeletal or non-cytoskeletal proteins in Anterior Horn cells are damaged and accumulate to form aggregation of the filaments associated with BB.

  • Observation of the proximal portions of axons of Anterior-Horn cells in the human spinal cord.
    Cells Tissues Organs, 1990
    Co-Authors: Shoichi Sasaki, Shoichi Maruyama, Makoto Takeishi
    Abstract:

    The proximal portions of axons of large Anterior-Horn cells were investigated in the lumbar cords of 10 normal human autopsy cases. Light-microscopically, 81 myelinated axons were observed to be conne

Mamede De Carvalho - 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.

  • 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.