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  • Neurofibrillary tangles  (11)
  • Hemispheric specialization  (2)
  • Neurodegenerative disorders  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Neuropathological observations in a case of autism presenting with self-injury behavior (1991)
    Springer
    Acta neuropathologica 82 (1991), S. 321-326 
    Details
    ISSN: 1432-0533
    Keywords: Autism ; Cerebral cortex ; Head trauma ; Neurofibrillary tangles ; Self-injury behavior
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the neuropathological evaluation of a 24-year-old autistic woman suffering from a residual state of infantile autism and presenting with self-injury behavior since childhood. Her behavior included head-banging, eye-gouging and self-biting. All intended therapeutic measures remained without effect, including high doses of psychotropic drugs. At autopsy, numerous neurofibrillary tangles were found in the perirhinal and entorhinal cortex where they were frequently grouped in nests or clusters. A few neurofibrillary tangles were also observed in the amygdala and in the prepiriform and orbito-frontal cortex. In the cortex, tangles were located in both layers II and III. There were no neuritic plaques or amyloid deposits. Interestingly, neurofibrillary tangles have been described in brains of individuals who had experienced repeated head injuries such as boxers (dementia pugilistica) and soccer players, suggesting that in our case a similar mechanism induced tangle formation and resulted in the loss of selective neuronal populations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00308819
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of cortical neurofibrillary tangles in progressive supranuclear palsy: A quantitative analysis of six cases (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 45-51 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Cerebral cortex ; Neurofibrillary tangles ; Progressive supranuclear palsy ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Progressive supranuclear palsy is characterized neuropathologically by the presence of high densities of neurofibrillary tangles in several subcortical structures. In some cases, neurofibrillary tangles have also been described in the cerebral cortex. We performed a quantitative regional and laminar analysis of the distribution of these lesions in six cases of progressive supranuclear palsy. We observed that the neurofibrillary tangle distribution in the cerebral cortex was largely confined to the hippocampal formation. In particular, in all the cases neurofibrillary tangles were observed in the granule cell layer of the dentate gyrus. In the prefrontal and inferior temporal cortex, neurofibrillary tangles were predominantly distributed in layers II and III. In addition, there were moderate-to-high neurofibrillary tangle densities in the primary motor cortex. This localization pattern contrasts with the neurofibrillary tangle distribution observed in the cerebral cortex of Alzheimer's disease cases, where tangles are denser in layer V than in layer III, and where the primary motor cortex and the dentate gyrus are usually not involved. These results suggest that specific elements of the cortical circuitry might be differentially vulnerable in progressive supranuclear palsy as compared to Alzheimer's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427214
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Alzheimer's disease with asymmetric atrophy of the cerebral hemispheres: morphometric analysis of four cases (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 440-447 
    Details
    ISSN: 1432-0533
    Keywords: Key words Senile plaques ; Neurofibrillary tangles ; Dementia ; Cortical atrophy ; Hemispheric specialization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the clinicopathological correlations in rare Alzheimer's disease patients with asymmetric cerebral atrophy and to compare their pattern of cortical involvement by senile lesions with that observed in other cases with atypical Alzheimer's disease, we performed an extensive neuropathological analysis of the cerebral cortex in four such cases. Three patients presented with severe language impairment but relatively good preservation of praxis and gnosis even after several years of clinical evolution. Cerebral autopsies of these cases revealed a predominant left hemisphere atrophy. Conversely, in one case with marked right hemisphere atrophy, all of the cognitive functions were involved early in the course of dementia. Neurofibrillary tangles and senile plaques were preferentially localized in the prefrontal, temporal and posterior parietal cortex in both hemispheres, whereas the hippocampal formation displayed lower lesion densities than neocortical areas. Significantly higher neurofibrillary tangle and senile plaque densities were found in the more atrophic side in most of the areas studied. The ratio of neurofibrillary tangle and senile plaque densities between the two hemispheres was not correlated with the number of these lesions in the cerebral cortex. These results indicate that the degenerative process in demented cases with interhemispheric asymmetric cerebral atrophy is characterized by a widespread involvement of the neocortex by senile lesions and lacks clear regional topography of neurofibrillary tangle and senile plaque distribution. Moreover, the relative sparing of the hippocampus, comparable to that found in cases with focal progressive dementia, suggests that the dementing process may involve different cortical structures in cases with asymmetric cerebral atrophy than in typical Alzheimer's disease cases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00389496
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Hyperphosphorylated tau proteins differentiate corticobasal degeneration and Pick’s disease (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 351-359 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cytoskeleton ; Microtubule-associated ; proteins ; Neurodegenerative disorders ; Protein ; phosphorylation ; Western blotting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In neurodegenerative disorders, hyperphosphorylated tau proteins aggregate into abnormal filaments. In the present study, tau protein alterations were studied in one corticobasal degeneration and seven Pick’s disease cases using specific immunological probes. The typical lesions of corticobasal degeneration and Pick’s disease were revealed by immunohistochemistry, including the presence of Pick bodies and achromatic swollen neurons, neuritic alterations, and neurofibrillary tangles. Tau-immunoreactive glial tangles were also observed. By immunoblotting, the case of corticobasal degeneration was characterized by the tau profile previously reported to occur in progressive supranuclear palsy with an intense labeling of the two tau 64 and 69 bands, while tau 55 was not visualized. In Pick’s disease cases with Pick bodies and neurofibrillary tangles, a tau triplet similar to that encountered in Alzheimer’s disease (tau 55, 64 and 69) was detected. Furthermore, a particular tau profile was found in four Pick’s disease cases showing only Pick bodies and no neurofibrillary tangles. In these cases, tau 55 and 64 were strongly immunoreactive, whereas tau 69 was almost unlabeled. These differences are likely to be related to particular pools of tau isoforms present within the degenerating neurons. Since there is a great diversity of neurodegenerative disorders with substantial clinical and neuropathological overlap, the electrophoretic profile of tau proteins could represent a useful marker for the type of neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050436
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Posterior cortical atrophy in Alzheimer's disease: analysis of a new case and re-evaluation of a historical report (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 215-223 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Balint's syndrome ; Corticocortical projections ; Neurofibrillary tangles ; Posterior cortical atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Disturbances of visual function are not uncommon in Alzheimer's disease and several cases with complex impairment of visuospatial abilities have been described. For instance, posterior cortical atrophy has been demonstrated in cases displaying Balint's syn-drome as the first symptom of the dementing illness. Such cases showed very high lesion counts in the occipital cortex, as well as in visual association regions in the posterior parietal and posterior cingulate cortex, whereas the prefrontal cortex was consistently less severely involved than usually observed in Alzheimer's disease. This suggests that the distribution of the lesions had been shifted to specific elements of the visual system. In the present study; we report the quantitative analysis of a new case of Alzheimer's disease with possible Balint's syndrome and re-evaluate a case originally described in 1945. The distribution of lesions in these two cases parallels previous observations of Alzheimer's disease cases with early visual impairment. Both cases displayed very high densities of neurofibrillary tangles and senile plaques in the primary visual cortex, secondary visual cortex, visual association areas of the dorsal occipital and posterior parietal lobe and in the posterior cingulate cortex, whereas the prefrontal and inferior temporal regions were comparatively less affected. These cases may define clinical subgroups of Alzheimer's disease and suggest that the breakdown of corticocortical projections that is known to occur in dementia may involve select components of specific functional systems in certain cases. In particular, path-ways that subserve motion detection and visuospatial analysis appear to be dramatically affected in these cases presenting with Balint's syndrome. Thus, Alzheimer's disease may be a more heterogeneous disorder than previously thought, and refined neuropsychological testing as well as detailed neuropathological evaluation may be of value to detect possible clinical variants of this dementing conditon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00304135
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  • 6
    Electronic Resource
    Electronic Resource
    Cellular distribution of the iron-binding protein lactotransferrin in the mesencephalon of Parkinson’s disease cases (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 566-572 
    Details
    ISSN: 1432-0533
    Keywords: Key words Ferritin ; Free radicals ; Oxidative stress ; Neurodegenerative disorders ; Transferrins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in the distribution of the iron-binding protein lactotransferrin have recently been described in the central nervous system during a variety of neurodegenerative disorders. To investigate whether lactotransferrin is associated with the neuropathological changes that characterize Parkinson’s disease, we analyzed the distribution of this protein in the mesencephalon of neurologically normal individuals and patients affected with Parkinson’s disease using quantitative immunohistochemical methods. High levels of lactotransferrin were observed in a large population of neurons in the substantia nigra of control cases. Lactotransferrin-positive neurons were severely affected by the neurodegenerative process that occurs in Parkinson’s disease as indicated by a severe decrease in the number of immunolabeled neurons in all of these cases. Quantitative analysis also demonstrated higher immunolabeling levels of lactotransferrin in the surviving neurons in the substantia nigra and ventral tegmental area of Parkinson’s disease cases compared to control cases. These results suggest that lactotransferrin may participate actively in the mechanism of neuronal degeneration in Parkinson’s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050468
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  • 7
    Electronic Resource
    Electronic Resource
    Phosphorylated serine422 on tau proteins is a pathological epitope found in several diseases with neurofibrillary degeneration (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 221-230 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neurodegenerative disorders ; Neurofibrillary tangles ; Phosphorylation ; Serine422 ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neuronal inclusions with bundles of abnormal filaments made of tau polymers are found in numerous diseases with neurofibrillary degeneration. Tau proteins are the basic components of paired helical filaments (PHF) in Alzheimer’s disease (AD), and are abnormally phosphorylated. A disease-specific phosphorylation site at serine422 was demonstrated on PHF, but not on tau proteins from biopsy-derived brain samples. In the present study, we report the characterization of a polyclonal antibody (988) against the serine422 phosphorylation site. By using biochemical and immunohistochemical methods, we confirmed that it is not found on tau proteins from biopsy- or autopsy-derived control samples, and we investigated the presence of this epitope on tau proteins in several neurodegenerative disorders, including AD, Down syndrome (DS), Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS/PDC), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), postencephalitic parkinsonism (PEP) and Pick’s disease (PiD). By Western blotting, antibody 988 labeled the characteristic tau triplet (tau 55, 64, 69) in AD, DS, Guamanian ALS/PDC and PEP. PSP and CBD exhibited their typical tau doublet (tau 64, 69), whereas the doublet tau 55 and 64 was detected in PiD. In all of these neurodegenerative disorders, antibody 988 clearly labeled NFT and dystrophic neurites, as well as Pick bodies in PiD cases, whereas no staining was observed in control cases. These data indicate that phosphorylation of serine422 on tau proteins is a common feature among neurodegenerative disorders and is therefore not specific of AD. Moreover, phosphorylation of this epitope permits the distinction between normal tau proteins and pathological tau proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050978
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  • 8
    Electronic Resource
    Electronic Resource
    Clinical validity of Braak neuropathological staging in the oldest-old (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 579-582 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Clinicopathological correlations ; Cognitive impairment ; dementia ; Neurofibrillary tangles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Several studies have demonstrated a good correlation between clinical severity and Braak’s neuropathological staging in Alzheimer’s disease (AD). However, nonagenarians and centenarians display a different pattern of cortical vulnerability to the neurodegenerative process compared to younger elderly, and it is not known whether correlations between clinical severity and neuropathological stages remain valid in this age group. To address this issue we compared Clinical Dementia Rating scale (CDR) scores and Braak stages in 116 patients over 90 years of age with either no cognitive impairment or very mild to severe AD. There is a strong positive correlation between CDR scores and Braak staging (Spearman coefficient = 0.66; P 〈 0.01). However, neuropathological staging does not distinguish cases with normal cognition (CDR 0) from those with mild cognitive changes (CDR 0.5). Unlike younger cohorts, Braak stages I and II are frequently associated with questionable dementia in this age group. Braak stage III overlaps with all CDR levels and correlates poorly with cognitive function. Braak stages IV or greater are consistently associated with at least mild dementia. Consistent with our previous neuropathological analyses of nonagenarians and centenarians, the present data suggest that the substantial involvement of the hippocampus which characterizes Braak stage IV is a key step in the development of overt clinical signs of dementia in the oldest-old. Moreover, they indicate that Braak staging represents a broad concept of the evolution of neurofibrillary tangles rather than a precise hierarchical model associated with a stepwise deterioration of cognitive abilities near the upper limit of life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051163
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  • 9
    Electronic Resource
    Electronic Resource
    Alzheimer's disease with asymmetric atrophy of the cerebral hemispheres: morphometric analysis of four cases (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 440-447 
    Details
    ISSN: 1432-0533
    Keywords: Senile plaques ; Neurofibrillary tangles ; Dementia ; Cortical atrophy ; Hemispheric specialization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the clinicopathological correlations in rare Alzheimer's disease patients with asymmetric cerebral atrophy and to compare their pattern of cortical involvement by senile lesions with that observed in other cases with atypical Alzheimer's disease, we performed an extensive neuropathological analysis of the cerebral cortex in four such cases. Three patients presented with severe language impairment but relatively good preservation of praxis and gnosis even after several years of clinical evolution. Cerebral autopsies of these cases revealed a predominant left hemisphere atrophy. Conversely, in one case with marked right hemisphere atrophy, all of the cognitive functions were involved early in the course of dementia. Neurofibrillary tangles and senile plaques were preferentially localized in the prefrontal, temporal and posterior parietal cortex in both hemispheres, whereas the hippocampal formation displayed lower lesion densities than neocortical areas. Significantly higher neurofibrillary tangle and senile plaque densities were found in the more atrophic side in most of the areas studied. The ratio of neurofibrillary tangle and senile plaque densities between the two hemispheres was not correlated with the number of these lesions in the cerebral cortex. These results indicate that the degenerative process in demented cases with interhemispheric asymmetric cerebral atrophy is characterized by a widespread involvement of the neocortex by senile lesions and lacks clear regional topography of neurofibrillary tangle and senile plaque distribution. Moreover, the relative sparing of the hippocampus, comparable to that found in cases with focal progressive dementia, suggests that the dementing process may involve different cortical structures in cases with asymmetric cerebral atrophy than in typical Alzheimer's disease cases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00389496
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    Paper (German National Licenses)
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  • 10
    Electronic Resource
    Electronic Resource
    Neuropathological changes in the cerebral cortex of 1258 cases from a geriatric hospital: retrospective clinicopathological evaluation of a 10-year autopsy population (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 456-468 
    Details
    ISSN: 1432-0533
    Keywords: Senile plaques ; Neurofibrillary tangles ; Dementia ; Neocortex ; Clinicopathological correlations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the neuropathological and clinical characteristics of cerebral aging, we evaluated retrospectively a non-selected autopsy population of 1258 patients from the Geriatric Hospital of the University of Geneva School of Medecine. The prevalence of Alzheimer's disease increased with age below 90 years of age. In the nonagenarians and centenarians, there was a decline in the number of affected cases. The distribution with age of neurofibrillary tangles and senile plaques varied among the cortical areas studied. The CA1 field of the hippocampus and the inferior temporal cortex displayed increasing densities of neurofibrillary tangles with age, whereas the superior frontal and the occipital cortex were relatively spared, especially in patients in their tenth and eleventh decade. The percentage of cases presenting with senile plaques in the neocortex and hippocampal structure increased with age with a marked predominance of cases with moderate to high senile plaque densities. Neurofibrillary tangles were often observed in the CA1 field and the inferior temporal cortex of non-demented individuals and were present in most cases with Alzheimer's disease. Conversely, the involvement of the superior frontal and occipital cortex was moderate even in demented patients. The distribution of senile plaques was homogeneous in all of the neocortical areas independently of the clinical diagnosis. Moreover, there was no correlation between the presence of heurofibrillary tangles and senile plaques in the cerebral regions studied. These results indicate a differential topography of neurofibrillary tangles and senile plaques, and suggest that overt clinical signs of Alzheimer's disease are linked to the progression of the neurodegenerative process in neocortical areas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294172
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