Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Parkinson’s disease: affection of brain stem nuclei controlling premotor and motor neurons of the somatomotor system (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 489-495 
    Details
    ISSN: 1432-0533
    Keywords: Key words Parkinson’s disease ; α-Synuclein ; Limbic ¶system ; Motor system ; Reticular formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pathological changes which consistently develop in the lower brain stem of patients suffering from Parkinson’s disease are described against the background of the internal organization and interconnections of the involved nuclei, i.e., the gigantocellular reticular nucleus, bulbar raphe nuclei, and coeruleus-subcoeruleus area. Immunoreactions against the presynaptic protein α-synuclein reveal not only the voluminous forms of Lewy bodies and Lewy neurites but also the otherwise inconspicuous dot- or thread-like types. These lesions develop solely in specific neuronal types. Lipofuscin- or neuromelanin-laden projection cells which at the same time generate a long, unmyelinated or sparsely myelinated axon are particularly susceptible to developing the changes. The bulbar nuclei under consideration receive strong input from supramedullary sources, above all from higher order centers of the limbic system such as the central amygdalar nucleus, periaqueductal gray, and parabrachial nuclei. In turn, they generate descending projections to premotor and motor neurons of the somatomotor system. The disease-related deterioration of both the supramedullary limbic centers and the bulbar brain stem nuclei reduces the limbic influence and markedly impairs the control of premotor and motor neurons. This functional deficit most probably contributes to the overall dysfunction of the motor system typically evolving in the course of Parkinson’s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051150
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Evolution of Alzheimer’s disease-related cytoskeletal changes in the basal nucleus of Meynert (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 259-269 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Basal nucleus of Meynert ; Neuronal cytoskeleton ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the evolution of Alzheimer’s disease (AD)-related pathology in a subcortical predilection site, the basal nucleus of Meynert (bnM), which is a major source of cortical cholinergic innervation. Brains of 51 autopsy cases were studied using silver techniques and immunostaining for tau-associated neurofibrillary pathology and for amyloid β protein (Aβ) deposits. All cases are classified according to a procedure permitting differentiation of six stages of AD-related neurofibrillary changes in the cerebral cortex. Initial cytoskeletal abnormalities in the bnM are already noted in stage I of cortical neurofibrillary changes. The gradual development of the neurofibrillary pathology in the bnM parallels the progression of the AD-related stages in the cerebral cortex. A variety of morphologically distinguishable cytoskeletal alterations are observed in large nerve cells which predominate in the bnM. Based on these cellular alterations, a sequence of cytoskeletal deterioration is proposed. Initially, the abnormal tau protein is distributed diffusely throughout the cell body and the neuronal processes. Subsequently, it aggregates to form a neurofibrillary tangle, which appears as a spherical somatic inclusion. The cell processes gradually become fragmented. Finally the parent cell dies, leaving behind an extraneuronal “ghost tangle”. With regard to the cortical stages of AD-related ¶neurofibrillary changes, the initial forms of cytoskeletal changes in the bnM predominate in the transentorhinal AD stages (I and II), while “ghost tangles” preferentially occur in the neocortical stages (V and VI). The considerable morphological diversity of cytoskeletal alterations is typical of stages III and IV. These results indicate that individual neurons of the bnM enter the sequence of cytoskeletal deterioration at different times.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004019900178
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Abstracts (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 1127-1166 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01273325
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Nerve cell loss in the thalamic centromedian-parafascicular complex in patients with Huntington's disease (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 161-168 
    Details
    ISSN: 1432-0533
    Keywords: Key words Huntington's disease ; Human brain ; Thalamus ; Nuclei centromedianus-parafascicularis ; Neurone number
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The centromedian-parafascicular complex represents a nodal point in the neuronal loop comprising striatum – globulus pallidus – thalamus – striatum. Striatal neurone degeneration is a hallmark in Huntington's disease and we were interested in estimating total neurone and glial number in this thalamic nuclear complex. Serial 500-μm-thick gallocyanin-stained frontal sections of the left hemisphere from six cases of Huntington's disease patients (three females, three males) and six age- and sex-matched controls were investigated applying Cavalieri's principle and the optical disector. Mean neurone number in the controls was 646,952 ± 129,668 cells versus 291,763 ± 60,122 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.001). Total glial cell number (astrocytes, oligodendrocytes, microglia, and unclassifiable glial profiles) was higher in controls with 9,544,191 ± 3,028,944 versus 6,961,989 ± 2,241,543 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.021). Considerable increase of fibrous astroglia within the centromedian-parafascicular complex could be observed after Gallyas' impregnation. Most probably this cell type enhanced the numerical ratio between glial number and neurone number (glial index: Huntington's disease patients = 24.4 ± 8.1; controls = 15.0 ± 5.2; Mann-Whitney U-test, P 〈 0.013). The neurone number in the centromedian-parafascicular complex correlated negatively, although statistically not significantly, with the striatal neurone number. This lack of correlation between an 80% neuronal loss in the striatum and a 55% neurone loss in the centromedian-parafascicular complex points to viable neuronal circuits connecting the centromedian-parafascicular complex with cortical and subcortical regions that are less affected in Huntington's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050408
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Argyrophilic grain disease is associated with apolipoprotein E ε2 allele (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 222-224 
    Details
    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
    URL: http://dx.doi.org/10.1007/s004010050886
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Neuroanatomie des Morbus Parkinson Veränderungen des neuronalen Zytoskeletts in nur wenigen für den Krankheitsprozess empfänglichen Nervenzelltypen führen zur progredienten Zerstörung umschriebener Bereiche des limbischen und des motorischen Systems (2000)
    Springer
    Der Nervenarzt 71 (2000), S. 459-469 
    Details
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Morbus Parkinson ; Motorisches System ; Limbisches System ; Lewy-Körper ; Lewy-Neuriten ; Zytoskelett ; α-Synuklein ; Key words Parkinson's disease ; Motor system ; Limbic system ; Lewy bodies ; Lewy neurites ; Cytoskeleton ; α-Synuclein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Morbus Parkinson is a progressive degenerative disease of the human central, peripheral, and enteric nervous systems. In the course of the disease, not only the substantia nigra, but also extranigral components of the motor system, as well as numerous limbic system and autonomic centers undergo serious damage. Accordingly, Parkinson's disease is a multisystem disorder. Only specific types of projection neurons fall victim to it. The first manifestation of the pathological process which causes the disease are abnormalities of the neuronal cytoskeleton. Intracytoplasmic inclusions evolving in the form of Lewy bodies in perikarya and Lewy neurites in the neuronal processes result in premature cell death of the affected neurons. On the basis of this selective neuronal vulnerability, a categorization emerges of the pathological changes within the nervous system and corresponding functional impairments.
    Notes: Zusammenfassung Der Morbus Parkinson ist eine stetig voranschreitende degenerative Erkrankung des zentralen, peripheren und enterischen Nervensystems des Menschen. Im Verlauf der Erkrankung erleiden neben der Substantia nigra eine Reihe von extranigralen Komponenten des motorischen Systems sowie zahlreiche Zentren des limbischen Systems und der autonomen Regulation schwerwiegende Zerstörungen. Der Morbus Parkinson ist daher eine Multisystemerkrankung. Nur bestimmte Arten von Projektionsneuronen entwickeln die für die Erkrankung charakteristischen Veränderungen des neuronalen Zytoskeletts. Das Ergebnis dieser Veränderungen sind intraneuronale Einschlusskörper in Form von Lewy-Körpern in den Zellleibern und Lewy-Neuriten in den Zellfortsätzen, die zum vorzeitigen Absterben der betroffenen Nervenzellen führen. Aufgrund der selektiven neuronalen Vulnerabilität ergibt sich eine charakteristische Verteilung der Veränderungen innerhalb des Nervensystems mit entsprechenden Einbußen der Funktionsfähigkeit zahlreicher Systeme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001150050607
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Nerve cell loss in the thalamic mediodorsal nucleus in Huntington’s disease. II. Optimization of a stereological estimation procedure (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 623-628 
    Details
    ISSN: 1432-0533
    Keywords: Key words Computer simulation ; Counting methods ; Disector ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study provides the theoretical background of the decision to count approximately 750–1,300 neurons per individual in the preceding study of Heinsen et al. [6] finding a significant (P 〈 0.05) nerve cell loss in the thalamic mediodorsal nucleus in Huntington’s disease with the so-called VRef× NV method. Using a computer simulation of the study of Heinsen et al., it was shown that the legitimation for counting only 100–200 neurons per individual in previous studies comparable to that carried out by Heinsen et al. was based on incorrect assumptions. In this context it was of particular importance to confirm the theoretical prediction in the literature that the random error of total neuron number estimates obtained with the VRef× NV method is actually greater than assumed in current stereological studies. In summary, this study revives the question of how many individuals need to be investigated and how many neurons (or other cell types, respectively) need to be counted per individual in studies comparable to that carried out by Heinsen et al.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051038
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Nerve cell loss in the thalamic mediodorsal nucleus in Huntington’s disease (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 613-622 
    Details
    ISSN: 1432-0533
    Keywords: Key words Human brain ; Thalamus ; Myeloarchitectonic ; Nerve cell number ; Optical disector
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We estimated the total neurone number, glial number, and glial index (ratio glial cells/neurone) in the thalamic mediodorsal nucleus (MD) in seven patients suffering from Huntington’s disease (HD; four males, three females, mean age 52.4 ± 13.6 years) and age- and sex-matched controls (four males, three females, mean age 53.6 ± 12.1 years) by means of a stereological protocol. The mean total neurone number (NT¯) in the MD of controls was 2,985,188 ± 174,710, the mean glial number (GT¯; astrocytes, oligodendrocytes) 21,785,008 ± 2,986,678, and the glial index 7.29 ± 0.88. In HD, the average neurone number was decreased by 23.8% to 2,275,321 ± 247,162 (Mann-Whitney U-test P 〈 0.05), the mean glial number by 29.7 % to 15,318,895 ± 1,722,524 (Mann-Whitney U-test P 〈 0.05), the glial index was slightly reduced to 6.81 ± 1.06. Gallyas’ impregnation for the demonstration of fibrous astroglia gave strongly positive results in all cases with HD and negative results in the controls. The morpho-functional correlation of the results is complicated because individual variability, presence of segregated and parallel neuronal circuits, and plasticity of the adult human CNS must be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051037
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...