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  • 1
    Electronic Resource
    Electronic Resource
    Discrepancy between tau immunoreactivity and argyrophilia by the Bodian method in neocortical neurons of corticobasal degeneration (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 553-557 
    Details
    ISSN: 1432-0533
    Keywords: Key words Corticobasal degeneration ; Tau ; Bodian ; stain ; Neurofibrillary tangles ; Pretangles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To clarify different features of cytoskeletal pathology in neocortical neurons between corticobasal degeneration (CBD) and Alzheimer’s disease (AD), the relationship between neurofibrillary tangles (NFTs), which are defined as a fibrillary structure stained by the Bodian method, and tau-immunopositive neurons in layers II–III of the premotor cortex was assessed by sequential staining for tau immunohistochemistry followed by the Bodian method on the same section. In AD brains, tau-like immunoreactivity in neurons was uniformly colocalized with Bodian-positive NFTs. In CBD brains, however, tau-immunopositive neurons could be classified into three different types: (1) those not stained at all by the Bodian method (diffuse cytoplasmic type), which represented the majority of these immunopositive neurons, (2) some partly stained by the Bodian method (mixed type), and (3) a few for which argyrophilia demonstrated by the Bodian method was completely colocalized with immunoreactivity (NFT type). This discrepancy between tau-like immunoreactivity and Bodian method is characteristic of CBD and suggests that the tau molecule is less liable to form argyrophilic fibrils in neocortical neurons of CBD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050934
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of cerebral cortical lesions in corticobasal degeneration: a clinicopathological study of five autopsy cases in Japan (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 416-424 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cerebral cortical lesion ; Clinicopathological correlation ; Corticobasal degeneration ; Pick’s disease ; Progressive supranuclear palsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated five Japanese patients with autopsy-proven corticobasal degeneration (CBD) both clinically and pathologically, and examined the distribution of their cerebral cortical lesions in hemisphere specimens. The lesions were classified into three categories (slight, moderate and severe). Only two of our patients had clinical features considered to be typical of CBD. Severe lesions were present in the posterior portions of the frontal lobe, anterior to the precentral gyrus in two patients with the clinical diagnosis of CBD. By comparison, in two patients with clinically diagnosed frontal Pick’s disease, and one with the clinical diagnosis of progressive supranuclear palsy (PSP), severe lesions were seen in the anterior portions of the frontal lobe. The primary motor area of all five had mostly slight to moderate lesions. We postulate that the clinical features of CBD have a much wider spectrum than previously believed. Our data also indicate that the lesion responsible for limb-kinetic apraxia in CBD is in the premotor cortex. We suggest that when the anterior portions of the frontal lobe are damaged, the clinical picture mimics those of Pick’s disease and PSP. In addition, we consider that focal cerebral atrophy of CBD is multicentric.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050728
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Prion disease with 144 base pair insertion in a Japanese family line (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 80-86 
    Details
    ISSN: 1432-0533
    Keywords: Prion protein ; Prion disease ; Insert mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe an insert mutation in the prion protein (PrP) gene in a Japanese family line that encodes six octapeptide repeats. This is the second report to date of an inherited prion disease with a 144-base pair insertion, although the order of the repeat sequences differ from that reported for the disease in an English family line. The clinical features, like those in the English patients, were characterized by a slowly progressive generalized dementia with some neurological signs and cortical focal symptoms. Postmortem examination disclosed diffuse atrophy of cerebral gray matter and the cerebellar cortex; histologically, there were marked patchy and regional neuronal loss with astrocytosis in the frontal cortex, amygdala and hippocampus and PrP-immunoreactive plaques in the molecular layer of the cerebellum. These plaques were different from typical kuru plaques. The prion disease in the present Japanese family line is compared with that in the English family line.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294463
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Variable Deposition of Amyloid β-Protein (Aβ) with the Carboxy-Terminus that Ends at Residue Valine40 (Aβ40) in the Cerebral Cortex of Patients with Alzheimer's Disease: A Double-Labeling Immunohistochemical Study with Antibodies Specific for Aβ40 and the Aβ that Ends at Residues Alanine42/Threonine43 (Aβ42) (1997)
    Springer
    Neurochemical research 22 (1997), S. 1499-1506 
    Details
    ISSN: 1573-6903
    Keywords: Diffuse deposits ; amyloid angiopathy ; senile plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Amyloid β-protein (Aβ) deposits in the cerebral cortices of patients with Alzheimer's disease (AD) were investigated immunohistochemically to determine their carboxy terminal sequences. Antibodies specific for Aβ terminating at residue valine40 (Aβ40) and at residues alanine42/threonine43 (Aβ42) were used. Virtually all parenchymal Aβ deposits were positive for Aβ42. Many of these deposits were also partially or completely labeled for Aβ40. The degree of Aβ40 labeling varied from area to area within a given brain and from AD case to AD case. In contrast to parenchymal deposits, Aβ40 labeled essentially all the vascular deposits which constitute amyloid angiopathy (AA), with Aβ42 occurring variably in some of these deposits. Occasional AA was found, however, in which Aβ42 predominated or was exclusively deposited. Such a diversity of Aβ species, both in brain parenchyma and in AA, suggests that multiple C-terminal processing mechanisms occur in the cell types responsible for these deposits.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1021910729963
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    Paper (German National Licenses)
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