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  • 1
    ISSN: 1432-0533
    Keywords: Key wordsα-Synuclein ; Filament pathology ; Lewy body ; NACP ; Tau
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The co-localization of NACP/α-synuclein and tau epitopes was examined in the brain stem and hippocampal formation in two patients from a family of autosomal dominant parkinsonism and dementia with Lewy bodies (LBs) without two reported missense mutations in the NACP gene. Double-labeling immunofluorescence study revealed that some brain stem LBs, cortical LBs, pale bodies, Lewy-related neurites, and neurofibrillary tangles expressed both NACP epitopes and the PHF tau AT8 epitope. Double-immunolabeling electron microscopy demonstrated that the NACP antibody selectively labeled 9- to 13-nm-thick straight filaments (LB filaments), whereas AT8 recognized twisted tubules with 80- to 100-nm-interval constrictions in the same neuronal inclusions. We show that NACP and tau aggregate into different filamentous components even if both proteins are incorporated into the same inclusions.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 53 (1981), S. 227-235 
    ISSN: 1432-0533
    Keywords: 6-Aminonicotinamide ; Aging ; Spinal cordd ; Neurons ; Neuroglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Following a single i.p. injection of 6-AN (10 mg/kg), the anterior horn cells of 20- and 25-month-old rats increased more in size and recovered slower from chromatolytic changes than those of 3-month-old rats. Neurofilamentous hyperplasia of the perikarya was more prominent in aged rats; proliferated neurofilaments were arranged in thick parallel bundles. In the acute stage, reactive and degenerative changes of glial and mesenchymal elements were more conspicuous in 3-month-old rats; however, they disappeared by day 14 with prominent proliferation of hypertrophic astrocytes. The older rats showed less intensity and slower progression of these changes; sponginess and swelling of the astrocytic cytoplasm were still observed at day 14. Our results suggest that these age-dependent changes in the response to neurotoxins are not only induced on the neuron without mitotic phenomena after birth, but also on neuroglial cells. Furthermore, an alteration or reduction in the support of the neuron augments its intensified and delayed susceptibility to neurotoxins.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 61 (1983), S. 27-35 
    ISSN: 1432-0533
    Keywords: Thiamine ; Development ; Wernicke's Encephalopathy ; Postsynaptic dendrite
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pregnant and nursing Wistar rats were fed a thiamine-deficient diet, and their offspring were injected daily with pyrithiamine. The pathologic lesions in the suckling rats were examined at different times of development. There were distinct changes at 22 days of age, by which time the rats are weaned, and the morphogenesis of the cerebellum is almost completed. Before 22 days of age, there were no pathologic changes except for scattered petechial hemorrhages in the brain. After 22 days of age, acute pathologic changes were observed, in decreasing order of severity, in the vestibular nuclei, inferior olivary nuclei, mammillary body, periventricular gray matter, thalamus, and quadrigeminal plates. The initial changes were swelling of postsynaptic dendrites and distension of the periaxonal space of myelinated axons in the parenchyma and ringshaped hemorrhages in the perivascular space. Pyrithiamine injections into the offspring of rats fed a thiamine-deficient diet probably induce disturbance of the electrolyte permeability of the neuronal excitable membrane, resulting in swelling of this element. These changes were followed by the infiltration of erythrocytes and plasma into the parenchyma and astrocytic swelling, which may be a secondary effect of neuronal changes on the rain vascular permeability.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 49 (1980), S. 19-27 
    ISSN: 1432-0533
    Keywords: 6-Aminonicotinamide ; Aging ; Spongy state ; Neuronal chromatolysis ; Pellagra ; Creutzfeldt-Jakob disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lesions in the CNS induced by 6-aminonicotinamide (6-AN) presented a spongy state of the gray matter and neuronal chromatolysis. With aging of the experimental animals the lesions extended from the phylogenetically early developed structures to those developed later, i.e., from spinal gray matter, dentate nuclei, and brain stem nuclei through limbic structures and striatum to the cerebral cortex. Changes of the neurons were more prominent with aging. Lesions in the CNS of rats at the age, corresponding to the involutional period in the human, were similar to those of Creutzfeldt-Jakob disease (C-J disease) in the presenile age. In recent years, the resemblance between C-J disease and pellagra encephalopathy had been noted by several authors, and they resemble the lesions caused by 6-AN, an antimetabolite of nicotinamide used in our experiment. This evidence, therefore, has led to the hypothesis that dysfunction of NAD(H)- or NADP(H)-dependent enzymes in the CNS of the aged, even if not the primary cause, may be one possible pathogenetic factor of C-J disease.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Pellagra ; 6-Aminonicotinamide ; Cervical gray matter ; Neuronal chromatolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructure of neuronal chromatolysis and other lesions in the gray matter of the cervical cord due to 6-aminonicotinamide (6-AN) administration, an antinicotinamide, to rats, were followed up during a 35-days period. Neuronal chromatolysis which was prominent in the anterior horn cells in the acute stage, was completely recovered from via the temprary hyperchromasia of their cytoplasm. Their axons, however, which form the anterior nerve roots, did not show any particular changes throughout the whole period of the experiment. This evidence suggests that neuronal chromatolysis induced by 6-AN might not be the result of axonal damage, but was due to the direct action of 6-AN on the soma of the anterior horn cells. In addition, necrosis of the internuncial cells, various reactions of glial and mesenchymal elements and the spongy state of the neuropil in the laminae VI and VII of Rexed of the cervical gray matter were observed in the acute stage. They were later repaired by glia. These lesions are usually absent in the central nervous system of human cases with pellagra. It is considered that the findings with 6-AN simulate the central nervous lesions of pellagra in human, but some minor differences in pathology such as presence of severer lesions in glia and other elements in the experimental rats would probably be caused by additional factors such as drastic mode of action, probable difference in catabolism of nicotinamide and 6-AN, and so forth.
    Type of Medium: Electronic Resource
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