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  • 1
    Electronic Resource
    Electronic Resource
    Alzheimer-type pathology in melanin-bleached sections of substantia nigra (1995)
    Springer
    Journal of neurology 242 (1995), S. 485-489 
    Details
    ISSN: 1432-1459
    Keywords: Bleaching ; Gallyas method ; Melanin Pigment ; Neurofibrillary tangles ; Substantia-nigra
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bleaching of melanin prior to Gallyas staining enabled us to detect an unexpectedly large number of neurofibrillary tangles (NFTs; 62 and 50 NFTs in the upper and the lower substantia nigra, respectively, mostly in the neuronal cytoplasm of the medial zona compacta) in brains of patients who had had Alzheimer's disease. Amyloid-like deposits were quite scarce. In Alzheimer's disease it has been commonly observed that other subcortical nuclei projecting widely to the cerebral cortex also contain a large number of NFTs, although they have few amyloid deposits. In these subcortical nuclei retrograde degeneration may initially affect intraneuronal processes, leading to the preferential development of NFTs in the neuronal cytoplasm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00867417
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  • 2
    Electronic Resource
    Electronic Resource
    Increased CSF tau protein in corticobasal degeneration (1997)
    Springer
    Journal of neurology 245 (1997), S. 44-46 
    Details
    ISSN: 1432-1459
    Keywords: Key words Tau ; Corticobasal ; degeneration ; Cerebrospinal fluid ; Sandwich ELISA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using a sensitive sandwich enzyme-linked immunosorbent assay (ELISA) method, we measured the concentration of total tau protein in the cerebrospinal fluid (CSF) from nine patients with corticobasal degeneration (CBD) in comparison with 12 normal control subjects in order to assess its diagnostic value. The CSF concentration of tau in patients with CBD (0.69, 0.20 ng/ml: mean, SD) was higher than that in the normal controls (0.48, 0.14 ng/ml, P = 0.0076 unpaired t test). This increase in CBD patients may reflect widespread tau pathology in CBD, but should be interpreted with reserve as an aid to diagnosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004150050173
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  • 3
    Electronic Resource
    Electronic Resource
    White matter amyloid in Alzheimer's disease brain (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 51-56 
    Details
    ISSN: 1432-0533
    Keywords: Key wordsβ-Protein ; White matter ; Laser scanning microscopy ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Amyloid β-protein (Aβ) deposits in the white matter were investigated by the double immunohistochemical staining for Aβ and neuritic, glial or vascular components. Reactive astroglia and neurite abnormality were absent around Aβ deposits in the white matter (w-Aβ) even those with a core. The association of w-Aβ with blood vessels was not consistent. Aggregates of activated microglia were found to be the sole but a consistent accompaniment of Aβ deposits even in the absence of other components such as neuron, synapse, neurite abnormality and reactive astroglia, as observed in the white matter. This suggests that the aggregates of activated microglia most likely represent one of the factors promoting the process of Aβ deposition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294459
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  • 4
    Electronic Resource
    Electronic Resource
    White matter amyloid in Alzheimer's disease brain (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 51-56 
    Details
    ISSN: 1432-0533
    Keywords: β-Protein ; White matter ; Laser scanning microscopy ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Amyloid β-protein (Aβ) deposits in the white matter were investigated by the double immunohistochemical staining for Aβ and neuritic, glial or vascular components. Reactive astroglia and neurite abnormality were absent around Aβ deposits in the white matter (w-Aβ) even those with a core. The association of w-Aβ with blood vessels was not consistent. Aggregates of activated microglia were found to be the sole but a consistent accompaniment of Aβ deposits even in the absence of other components such as neuron, synapse, neurite abnormality and reactive astroglia, as observed in the white matter. This suggests that the aggregates of activated microglia most likely represent one of the factors promoting the process of Aβ deposition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294459
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Inconstant apolipoprotein E (ApoE)-like immunoreactivity in amyloid β protein deposits: relationship with APOE genotype in aging brain and Alzheimer’s disease (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 180-185 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E ; APOE genotype ; Alzheimer’s disease ; Senile plaque
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to analyze the relationship between apolipoprotein E (ApoE) and amyloid β-protein (Aβ) deposits in 29 brains from a series of elderly women, whose intellectual status had been prospectively assessed by the Blessed test score (BTS). In three cases the APOE genotype was ɛ3/4, in one ɛ2/2, in 25 ɛ3/3. ApoE-like immunoreactive lesions resembling a classic senile plaque (ApoE-SP) or a diffuse deposit (ApoE-DD) were quantitatively assessed in the first temporal gyrus (Brodmann’s area 22). The density of ApoE-positive deposits (ApoE-SP+ApoE-DD) was correlated with BTS (negative correlation R 2 = 0.36, P = 0.0006). The correlation of the density of ApoE-DD with BTS (R 2 = 0.26, P = 0.0051) was weaker than that of ApoE-SP (R 2 = 0.50, P 〈 0.0001). The density of ApoE deposits was correlated with that of Aβ-immunoreactive lesions (positive correlation R 2 = 0.57, P 〈 0.0001). ApoE immunohistochemistry labeled fewer deposits than Aβ immunohistochemistry but showed as many senile plaques (ApoE-SP) as tau immunohistochemistry and the Gallyas and Bodian techniques. Two of the three cases with the ɛ3/4 allele had Alzheimer’s disease (AD) with numerous ApoE-immunoreactive senile plaques. In contrast, the brain of the third ɛ3/4 case, whose intellectual status was normal, contained numerous Aβ deposits but lacked ApoE-like immunoreactivity. The presence of ApoE may, thus, not be a prerequisite for Aβ deposition, even in cases with the ɛ3/4 allele. The density of ApoE-SP peaked in layer III, whereas that of ApoE-DD was maximal in deeper cortical layers. This contrast in the laminar distribution indicates that only some ApoE-DD may evolve into ApoE-SP. ApoE deposition was linked to the intellectual decline and was constant in the most severely demented patients, in whom numerous ApoE-positive (and Aβ-positive) neuritic plaques were surrounded by dystrophic neurites. ApoE may accumulate in neuritic senile plaques during the progression of AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050506
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  • 6
    Electronic Resource
    Electronic Resource
    Widespread immunoreactivity of presenilin in neurons of normal and Alzheimer’s disease brains: double-labeling immunohistochemical study (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 325-330 
    Details
    ISSN: 1432-0533
    Keywords: Key words Presenilin ; Alzheimer’s disease ; Immunohistochemistry ; Golgi apparatus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The immunolocalization of presenilin in human brain was studied using two antibodies raised against different portions of presenilin 1 (S182) protein. A granular staining was found in the cytoplasm of neurons in cortical layers III and V. One of the antibodies, also reactive to presenilin 2 (E5-1) protein, additionally stained dendrites and axons. This was seen in normal brains as well as in brains affected by Alzheimer’s disease. Less prominent immunolabeling was noted in some senile plaques. No relationship to neurofibrillary tangles was found in double-labeling experiments combined with anti-paired helical filament-tau antibody (AT8). The widespread expression of presenilin in normal brain suggests a physiological role of the protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050526
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  • 7
    Electronic Resource
    Electronic Resource
    Paraneoplastic encephalo-myelo-ganglionitis: cellular binding sites of the antineuronal antibody (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 85-92 
    Details
    ISSN: 1432-0533
    Keywords: Paraneoplastic syndrome ; Encephalo-myelo-ganglionitis ; Antineuronal antibody ; Confocal laser-scanning microscopy ; Immunoelectron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cellular binding sites of an antineuronal antibody were characterized in an autopsy case of the paraneoplastic encephalo-myelo-ganglionitis. A 61 year-old woman developed a subacute sensorimotor polyneuropathy and, later, multiple involvement of cranial nerves, disturbance of consciousness, and generalized seizure. An autopsy revealed a small cell lung carcinoma and neuropathological changes that included disseminated encephalitis, spinal anterior horn lesions, severe loss of dorsal root ganglion neurons, and secondary degeneration and loss of the nerve fibers in the spinal posterior column and peripheral nerves. The serum IgG from the patient contained antineuronal antibody(s) including an antibody to 35- to 37-kDa neuronal antigens called anti-Hu as demonstrated in Western blot. In immunohistochemical studies, the serum IgG immunostained neurons of the brains, spinal cords, and dorsal root ganglia of humans or rats. Confocal laserscanning microscopy revealed binding of the patient's IgG in the neuronal nuclei and cytoplasm, but not in the nucleoli. In immunoelectron microscopic studies, immunolabelling with the IgG was found diffusely in the karyoplasm, excluding nucleoli, and in the cytoplasmic matrix between the cisternae of the reticulums, Golgi apparatus, and mitochondria. Encephalo-myeloganglionitis is a clinicopathological entity frequently associated with the presence of neoplasm and antineuronal antibody, however, the role of the antibody in the pathogenesis remains to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294364
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  • 8
    Electronic Resource
    Electronic Resource
    Dissociation of Alzheimer type pathology in a disconnected piece of cortex (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 501-507 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer disease ; Neuritic plaque ; β-Amyloid diffuse deposit ; Disconnection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A woman with Alzheimer’s disease died at the age of 85 years. A left sphenoid meningioma had been removed 27 years earlier. The tumor and the operation had severely altered the white matter of the frontal lobe and of the anterior part of the temporal lobe on the left side and massively disconnected a small piece of frontal cortex. There were numerous senile plaques and neurofibrillary tangles in the limbic and isocortical samples. The white matter lesions, on the operated (left) side, were associated with a lower density of neuritic plaques and of neuropil threads and with a higher density of β-amyloid (Aβ) deposits. The density of tau-positive neuritic plaques, neurofibrillary tangles and neuropil threads was close to zero, whereas the diffuse deposits of Aβ were abundant, in the small disconnected piece of cortex. In this area, the white matter was severely damaged, as in the adjoining cortex, but the continuity of the cortical ribbon was also disrupted. These data show that neuritic and Aβ pathologies may be dissociated and suggest that the neuritic alterations mainly involve cortico-cortical fibers coursing tangentially in the cortical ribbon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050645
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  • 9
    Electronic Resource
    Electronic Resource
    Tumor necrosis factor-α, microglia and astrocytes in AIDS dementia complex (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 508-517 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cytokine ; HIV-associated cognitive/motor complex ; Prospective study ; Immunohistochemistry ; Macrophages
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenesis of HIV-associated cognitive changes is poorly understood. Cytokines such as tumor necrosis factor-α (TNF-α) have been postulated to contribute to the mechanism of the neurological complications of HIV infection. One of the effects of TNF-α is to induce astrocyte proliferation in vitro. The purpose of this study was to look for a correlation between the expression of TNF-α, astrogliosis and the degree of cognitive impairment in 12 prospectively assessed AIDS cases without focal brain lesion, 8 of whom were demented. They were compared with 6 control patients without neurological disease. Neuropathological examination showed myelin pallor in 5 of the 8 demented patients. TNF-α expression was detected by immunohistochemistry in the midfrontal cortex, subcortical and deep white matter, and basal ganglia. Not only perivascular macrophages but also some microglial and endothelial cells were labeled. Most TNF-α-positive cells were in close contact with glial fibrillary acidic protein-positive astrocytes. They were more numerous than gp41-positive cells. Their density increased with increasing cognitive impairment and in parallel to the astrogliosis in the frontal cortex, basal ganglia and deep white matter. These findings further support the hypotheses that lesions of the deep white matter, driven by TNF-α, are associated with cognitive alteration, and that indirect effects of HIV infection in the brain participate in the development of HIV-associated dementia through a diffuse immune activation, mediated by cytokines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050646
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  • 10
    Electronic Resource
    Electronic Resource
    Atypical neuronal inclusion bodies in meningioangiomatosis (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 91-96 
    Details
    ISSN: 1432-0533
    Keywords: Key words Meningioangiomatosis ; Neurofibrillary ; tangles ; Lewy body ; Pick body
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A case of meningioangiomatosis not associated with neurofibromatosis 2 in a 24-year-old man is reported. Abundant neurofibrillary tangles and threads, shown by immunohistochemistry and ultrastructural analysis to be similar to those seen in Alzheimer’s disease, were found in the residual neuropil. Another lesion consisting of argyrophilic globular inclusion bodies with radial fibrils was found at the periphery. Single and double immunostaining with a panel of antibodies showed similarities between these inclusions and Pick bodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050864
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