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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 88 (1994), S. 493-500 
    ISSN: 1432-0533
    Keywords: Key words Amygdala ; Lewy body ; Parkinson's ; disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The amygdala undergoes severe pathological changes during the course of Parkinson's disease (PD). Lewy bodies and Lewy neurites are distributed in a specific manner throughout the nuclear complex. The lesional pattern displays only minor interindividual variation. The most prominent changes occur in the accessory cortical and central nuclei. The cortical, accessory basal and granular nuclei show less severe alterations, while the basal and lateral nuclei, as well as the intercalated cell masses, generally remain uninvolved. The amygdala receives a broad range of afferents, allowing integration of exteroceptive information with interoceptive data. It generates major projections to the isocortex (the prefrontal cortex in particular), limbic system (hippocampus and entorhinal region) and centers regulating endocrine and autonomic functions. The specific lesional pattern seen in PD destroys part of the nuclear gray matter and its connections and, thus, may likely contribute to the development of behavioral changes and autonomic dysfunctions.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 92 (1996), S. 197-201 
    ISSN: 1432-0533
    Keywords: Key words Oligodendrocytes ; Myelination ; Alzheimer’s disease ; Neurofibrillary tangles ; Neuropil ; threads
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pattern of neurofibrillary changes which gradually develops in the course of Alzheimer’s disease bears a striking resemblance to the inverse sequence of cortical myelination. Factors released by oligodendrocytes exert a strong influence upon nerve cells and suppress disordered neuritic outgrowth. It is suggested that the lack of such factors due to premature dysfunction of oligodendrocytes leads to alterations of the neuronal cytoskeleton and eventually to the appearance of Alzheimer-type neurofibrillary changes.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E genotype ; ɛ2 allele ; Argyrophilic grain disease ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Argyrophilic grain disease (AGD) is a distinct degenerative disorder of the human brain associated with the formation of abnormally phosphorylated tau protein. AGD-related cytoskeletal changes are known to affect specific subsets of nerve cells and oligodendrocytes. Here we demonstrate a remarkable association between the apolipoprotein E (ApoE) ɛ2 allele and AGD. Individuals afflicted with AGD (n = 48) reveal a significantly higher frequency of the ɛ2 allele compared with controls (n = 43) (22% versus 4%, P 〈 0.0002). The association between AGD and ɛ2 allele of ApoE suggests that AGD can be distinguished from other neurodegenerative disorders not only neuropathologically, but also genetically.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Anatomy and embryology 179 (1988), S. 165-172 
    ISSN: 1432-0568
    Keywords: Somatostatin-14 ; Human olfactory bulb ; Anterior olfactory nucleus ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study describes the morphological features and the distribution pattern of neurons in the human olfactory bulb which are immunoreactive for an antiserum against the neuropeptide somatostatin-14. Immunoreactive nerve cell bodies were mainly found in the white matter surrounding the cell clusters of the anterior olfactory nucleus. Some immunoreactive neurons were also found scattered throughout the anterior olfactory nucleus and the deeper parts of the inner granule cell layer. Only a few immunoreactive neurons were localized in the glomerular layer and the outer granule cell layer. Immunoreactive fibres were found in all layers of the olfactory bulb. In addition, an impressive number of coiled and kinked immunoreactive fibres were localized within the anterior olfactory nucleus forming a dense plexus. Accumulations of twisted and coiled branches of immunoreactive fibres were rarely found either surrounding or within the olfactory glomerula. The characteristics of somatostatin-14 immunoreactive neurons as seen in the combined pigment-Nissl preparation were studied after decolourizing the chromogen and restaining the preparations with aldehydefuchsin in order to demonstrate the lipofuscin pigment and gallocyanin chrome alum for Nissl material. About 90% of the immunoreactive neurons studied in this manner turned out to be devoid of lipofuscin granules. The remaining 10% displayed different patterns of pigmentation. These findings suggest the presence of different types of somatostatin-14-like immunoreactive neurons in the olfactory bulb of the human adult.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 77 (1989), S. 494-506 
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Amyloid ; Neuritic plaques ; Neurofibrillary tangles ; Neuropil threads
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sensitive and specific silver methods for demonstration of (1) amyloid and/or precursors of amyloid and (2) neurofibrillary changes were applied to examine the pathology revealed by the occipital isocortex in cases of Alzheimer's disease and age-matched controls. In general, amyloid and/or precursors of amyloid are encountered in plaque-like formations. Large numbers of amyloid plaques occur in layers that only occasionally harbor neuritic plaques. Amyloid deposits can be found in abundance in the occipital cortex of demented individuals exhibiting an only sparse number of neuritic plaques. In demented individuals the striate area contains almost as much amyloid as the parastriate area or the peristriate region. Neurofibrillary changes are encountered in neuritic plaques, neurofibrillary tangles, and neuropil threads. Neuritic plaques are predominantly found in layers II and III. Their density changes even within the boundaries of architectonic units. Large numbers of plaques are found in the cortex covering the depth of the sulci. The number of neurofibrillary tangles increases abruptly when passing the striate/parastriate and the parastriate/peristriate boundaries. The neuropil threads may densely fill a layer without the presence of neurofibrillary tangles (layer V of the striate area). Neuropil threads contribute a substantial part to the total amount of the intraneuronally deposited pathological material.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 82 (1991), S. 239-259 
    ISSN: 1432-0533
    Keywords: Amyloid ; Neurofibrillary changes ; Dementia ; Alzheimer's disease ; Stageing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre-α (transentorhinal stages I–II). The two forms of limbic stages (stages III–IV) were marked by a conspicuous affection of layer Pre-α in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V–VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 81 (1991), S. 261-268 
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Amyloid ; Neurofibrillary changes ; Thalamus ; Limbic system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sensitive silver techniques for amyloid and neurofibrillary changes were applied to examine the pathological changes revealed by limbic nuclei of the thalamus in Alzheimer's disease. Large numbers of extracellular amyloid deposits occurred in almost all thalamic nuclei. The antero-ventral nucleus harbored numerous large globular patches, other areas contained more densely packed and smaller deposits, while narrow zones of gray matter subjacent to the ependymal lining of the third ventricle remained virtually devoid of amyloid. Intraneuronal neurofibrillary changes were encountered in the form of distended argyrophilic processes covering the medial convexity of the antero-ventral nucleus. Similar structures, although in considerably lesser density, occurred in the laterally adjoining reticular nucleus. The anterior nuclear complex, the latero-dorsal nucleus, portions of the intralaminar complex, the paraventricular and reuniens nucleus contained numerous neurofibrillary tangles and neuropil threads. The antero-dorsal nucleus showed the most severe involvement. At first glance, the thalamus appeared to be only mildly affected by Alzheimer's disease. Closer inspection revealed that severe changes were confined to only a few limbic nuclei. These changes were virtually identical in amount, type and location in all cases of severe Alzheimer's disease studied. It is assumed that these changes considerably hamper the transport of information through limbic circuits.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Dementia ; Amyloid ; Neurofibrillary tangles ; Entorhinal region
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cases of old-aged demented individuals exhibited abundant cortical amyloid deposits but only small numbers of neurofibrillary changes. Neuritic plaques were rare or absent. Neither Ammon's horn nor isocortex revealed sufficiently large numbers of tangles to permit the diagnosis of fully developed Alzheimer's disease. Dense accumulations of neurofibrillary tangles and neuropil threads occurred only in layer Pre-α (II) of the entorhinal region. This pattern of cortical destruction may represent a variant of Alzheimer's disease or an initial stage of this disorder.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: KeyWordsCytoskeleton ; Neurofibrillary tangle Neuropil thread ; Tau protein ; Abnormal phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Frontal sections of the temporal lobe including the transentorhinal/entorhinal region, amygdala, and/or hippocampus from human adult brains are studied for cytoskeleton changes using immunostaining with the antibodies AT8 and Alz-50 and selective silver impregnation methods for neurofibrillary changes of the Alzheimer type. For the purpose of correlation, the two methods are carried out one after the other on the same section. Layer pre-α in the transentorhinal/entorhinal region harbours nerve cells which are among the first nerve cells in the entire brain to show the development of neurofibrillary changes. This presents the opportunity for study of both early events in the destruction of the cytoskeleton in individual neurons, and to relate changes which occur in the neuronal processes in the absence of alterations in their immediate surroundings to those happening in the soma. Immunoreactions with the AT8 antibody in particular reveal a clear sequence of changes in the neuronal cytoskeleton. Group 1 neurons present initial cytoskeleton changes in that the soma, dendrites, and axon are completely marked by granular AT8 immunoreactive material. These neurons appear quite normal and turn out to be devoid of argyrophilic material when observed in silver-stained sections. Group 2 neurons show changes in the cellular processes. The terminal tuft of the apical dendrite is replaced by tortuous varicose fibres and coarse granules. The distal protions of the dendrites are curved and show appendages and thickened portions. Intensely homogeneously immunostained rod-like inclusions are encountered in these thickened portions and in the soma. A number of these rod-like inclusions are visible after silver staining, as well. Group 3 neurons display even more pronounced alterations of their distal – most dendritic portions. The intermediate dendritic parts lose immunoreactivity, but the soma is homogeneously immunostained. Silver staining reveals in most of the distal dendritic parts neuropil threads, and in the soma a classic neurofibrillary tangle. Group 4 structures are marked by accumulations of coarse AT8-immunoreactive granules. Silver staining provides evidence that the fibrillary material has become an extraneuronal, “early” ghost tangle. Finally, group 5 structures present “late” ghost tangles in silver-stained sections but fail to demonstrate AT8 immunoreactivity. It is suggested that the altered tau protein shown by the antibody AT8 represents an early cytoskeleton change which eventually leads to the formation of argyrophilic neurofibrillary tangles and neuropil threads.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 93 (1997), S. 323-325 
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Neurofibrillary ; changes ; Abnormal tau protein ; Ammon’s horn
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the course of Alzheimer’s disease, specific CA1 pyramidal cells develop dendritic changes, which can only be observed transiently. Distal segments of the apical dendrite running through the stratum lacunosum-moleculare show spindle-shaped dilations filled with abnormal tau protein. The alteration eventually leads to amputation of the changed segment. The damage first appears at stage II in the evolution of the neurofibrillary changes [5], is best developed at stage III, and vanishes from the tissue at stage IV. It is usually not observed in stages V and VI (fully developed Alzheimer’s disease).
    Type of Medium: Electronic Resource
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