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  • 1
    Electronic Resource
    Electronic Resource
    Transferrin Receptor Expression and Iron Uptake in the Injured and Regenerating Rat Sciatic Nerve (1991)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 3 (1991), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Iron-saturated transferrin is a ubiquitous growth factor that plays a critical role in cellular iron uptake, growth and proliferation. Here we have studied the expression and distribution of transferrin receptors and iron uptake following injury of the rat sciatic nerve. Axotomy led to a massive but transient increase (days 2–9, maximum day 4) in [125l]transferrin binding at the site of the injury and in the distal, denervated part of the crushed or resected sciatic nerve, shortly preceding the time course of cellular proliferation (Friede and Johnstone, Acta Neuropathol, 7, 218–231, 1967; Jurecka et al., Acta Neuropathol, 32, 299–312, 1975). An additional, transient increase in specific binding was observed during reinnervation after reconnection of the resected sciatic nerve. Immunocytochemistry using the Ox-26 monoclonal antibody revealed strong and simultaneous expression of the transferrin receptor protein on two different cell types: on a subpopulation of blood-borne macrophages invading the injured peripheral nerve and on Schwann cells reacting to denervation and reinnervation. In addition, studies using intravenously injected radioactive iron (59Fe3+) showed a massive increase in endoneural iron uptake confined to the lesion site and to the distal part of the axotomised sciatic nerve, parallel to the time course of reactive transferrin receptor expression. Since iron is an essential cofactor of a number of key enzymes needed in energy metabolism and DNA synthesis, these data suggest that the induction of transferrin receptor expression may play an important role in the regulation of cellular growth and proliferation during peripheral nerve regeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1991.tb00027.x
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  • 2
    Electronic Resource
    Electronic Resource
    Apolipoprotein E genotype and neuropathological phenotype in two members of a German family with chromosome 14-linked early onset Alzheimer's disease (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 257-265 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyloid precursor protein gene ; Archival ; neuropathological tissue ; Mitochondrial NADH ; dehydrogenase subunit gene ND2 ; Polymerase chain ; reaction-based genomic sequencing ; Quantitative ; immunocytochemical analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Molecular genetic analysis was performed in two autopsy-confirmed cases of early-onset Alzheimer's disease belonging to a large German pedigree [FAD2, according to the nomenclature of St. George-Hyslop, et al. (1987) Science 235 : 885–890]. The disease in this family has been linked to chromosome 14. As gene interactions are considered to influence the age of onset and tissue pathology in Alzheimer's disease, we have studied three candidate genes that could modify disease progression. In this study a new polymerase chain reaction (PCR) assay was established for apolipoprotein E genotyping in archival neuropathological tissue, exon 17 of the amyloid precursor protein gene was directly sequenced, and a candidate mutation site at nucleotide (nt) 5460 of the mitochondrial NADH dehydrogenase subunit gene ND2 was analyzed employing PCR followed by HphI digestion. Whereas no sequence variations were detected in exon 17APP or at nt5460 of mitochondrial DNA, the apolipoprotein E genotypes of the two cases differed. Neuropathological examination revealed a higher number of βA4-positive amyloid plaques and a larger total tissue area covered by βA4 deposits in the ε3/ε3 homozygote. In contrast, the number of cortical neurofibrillary tangles and the number of plaques with tau-positive neurites appeared to be higher in the ε3/ε4 heterozygote. Our findings support the view that the chromosome 14 genetic defect, rather than apolipoprotein E genotype, is the preeminent factor determining Alzheimer's disease pathology in this family.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296509
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  • 3
    Electronic Resource
    Electronic Resource
    Unscheduled DNA synthesis and mitochondrial DNA synthetic rate following injury of the facial nerve (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 557-566 
    Details
    ISSN: 1432-0533
    Keywords: Key words Motoneuron regeneration ; DNA repair ; Mitochondrial DNA synthesis ; Neuronal regeneration ; [3H]Thymidine ; Autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unscheduled DNA synthesis (UDS) of nuclear DNA and mitochondrial (mt) DNA synthetic rates were determined autoradiographically in different cell types of the rodent brain 14 days after unilateral facial nerve transection. In addition to an increased synthetic rate of mtDNA in facial motoneurons 12 h after axotomy, a significant increase of UDS, i.e., DNA repair, and mtDNA synthesis were found in the regenerating facial nucleus 4 days after axotomy. Specificity of the observed labeling was confirmed by injection of 3H2O instead of [3H]thymidine. Using electron microscopic autoradiography, it was further shown that cytoplasmic labeling of neurons was mainly due to incorporation of radioactive label into mitochondria, indicating their subsequent multiplication by division. The observation that Northern blot signals for O6-alkylguanine-DNA-alkyltransferase mRNA from homogenized facial nuclei of both the axotomized and normal side remained unchanged over 14 days after axotomy indicated that the observed DNA-repair activity was not caused by endogenously produced alkylating agents. The combined presence of transiently increased UDS, enhanced mtDNA synthesis and elevated protein synthetic rates of regenerating motoneurons (as shown in the literature) suggests that free radicals produced by mitochondria in injured nerve cells could cause unspecific DNA damage followed by immediate repair.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050750
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  • 4
    Electronic Resource
    Electronic Resource
    Apolipoprotein E genotype and neuropathological phenotype in two members of a German family with chromosome 14-linked early onset Alzheimer's disease (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 257-265 
    Details
    ISSN: 1432-0533
    Keywords: Amyloid precursor protein gene ; Archival neuropathological tissue ; Mitochondrial NADH dehydrogenase subunit gene ND2 ; Polymerase chain reaction-based genomic sequencing ; Quantitative mmunocytochemical analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Molecular genetic analysis was performed in two autopsy-confirmed cases of early-onset Alzheimer's disease belonging to a large German pedigree [FAD2, according to the nomenclature of St. George-Hyslop, et al. (1987) Science 235:885–890]. The disease in this family has been linked to chromosome 14. As gene interactions are considered to influence the age of onset and tissue pathology in Alzheimer's disease, we have studied three candidate genes that could modify disease progression. In this study a new polymerase chain reaction (PCR) assay was established for apolipoprotein E genotyping in archival neuropathological tissue, exon 17 of the amyloid precursor protein gene was directly sequenced, and a candidate mutation site at nucleotide (nt) 5460 of the mitochondrial NADH dehydrogenase subunit gene ND2 was analyzed employing PCR followed by HphI digestion. Whereas no sequence variations were detected in exon 17APP or at nt5460 of mitochondrial DNA, the apolipoprotein E genotypes of the two cases differed. Neuropathological examination revealed a higher number of βA4-positive amyloid plaques and a larger total tissue area covered by βA4 deposits in the ε3/ε3 homozygote. In contrast, the number of cortical neurofibrillary tangles and the number of plaques with tau-positive neurites appeared to be higher in the ε3/ε4 heterozygote. Our findings support the view that the ahromosome 14 genetic defect, rather than apolipoprotein E genotype, is the preeminent factor determining Alzheimer's disease pathology in this family.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296509
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Formation of microglia-derived brain macrophages is blocked by adriamycin (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 348-358 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin ; Brain macrophages ; Microglia proliferation ; Motor neuron degeneration ; Ricinus communis lectin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Injection of ricin, the toxic lectin fromRicinus communis, into the rat facial nerve leads to rapid degeneration of motor neurons and concomitant proliferation and transformation of endogenous microglia into brain macrophages. Using [3H]-thymidine autoradiography, immunocytochemistry for microglial markers and electron microscopy, we could show that when ricin was administered together with the cytostatic drug adriamycin, the retrogradely transported adriamycin inhibits the macrophage response induced by toxic ricin. It is concluded that under conditions of neuronal degeneration, e.g., following ricin intoxication, brain macrophages are predominantly, if not exclusively, derived from endogenous microglia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688171
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  • 6
    Electronic Resource
    Electronic Resource
    Use of neuropathological tissue for molecular genetic studies: parameters affecting DNA extraction and polymerase chain reaction (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 19-25 
    Details
    ISSN: 1432-0533
    Keywords: DNA isolation ; Formalin fixation ; Genetic analysis ; Neurodegenerative disorders ; Paraflin embedding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nuclear and mitochondrial DNA were extracted from gray matter of human cerebral cortex which had either been formalin-fixed and embedded into paraffin or stored in formalin for up to 26 years. Extraction conditions were optimized for proteinase K digestion, i.e., enzyme concentration, digestion temperature and incubation time. Using the polymerase chain reaction (PCR), DNA was successfully amplified from archival material and sequenced employing a direct nonradioactive cycle sequencing protocol. In general, tissue embedded into paraffin following brief fixation in formalin gave good quantitative results, i.e., up to 1 μg DNA/mg tissue were extracted. This yield was at least one order of magnitude higher than that obtained with tissue stored in formalin. However, paraffin-embedded neuropathological material was found to contain an as-yet-unidentified PCR inhibitor, and a deleterious effect of long-term fixation in unbuffered low-grade formalin was clearly detectable. Importantly, both paraffin-embedded tissue blocks and human brain that had been stored in formalin for many years yielded DNA sufficient for qualitative analysis. The implications of these findings for the use of neuropathological material in molecular genetic studies are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294355
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  • 7
    Electronic Resource
    Electronic Resource
    Synaptic stripping in the human facial nucleus (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 179-181 
    Details
    ISSN: 1432-0533
    Keywords: Astrocytes ; Microglia ; Motor neuron ; Regeneration ; Synapses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of severe peripheral facial nerve paresis with disconnection of synapses from facial motor neurons is reported. A 77-year-old man presented with left-sided otitis media and subsequent development of facial nerve paresis. Three months later, the patient died of an acute gastrointestinal bleeding from a chronic duodenal ulcer. Gross inspection of the brain revealed non-stenosing arteriosclerotic vascular changes and a single small cystic lesion in the right putamen. Microscopically, marked chromatolytic changes were observed in the left facial nucleus. Immunocytochemistry for synaptophysin revealed a marked loss of afferent synaptic contacts from somatic and stem dendritic surface membranes of all chromatolytic motor neurons. Wrapping of a number of neurons by newly formed glial fibrillary acidic protein-positive astrocytic cell processes could be detected in the regenerting facial motor nucleus. In addition, expression of HLA-DR was increased on a small number of microglia and pertivascular cells. These changes were absent from the contralateral, normal-appearing facial nucleus. To our knowledge, this case provides the first evidence for disconnection of synapses following peripheral nerve lesioning in humans. Occurrence of synaptic stripping is likely to explain nuclear hyperexcitability and failure of recovery of complex fine motor movements that are commonly observed following peripheral injury to the facial nerve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334886
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  • 8
    Electronic Resource
    Electronic Resource
    On the question of apoptosis in the parkinsonian substantia nigra (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 105-108 
    Details
    ISSN: 1432-0533
    Keywords: Key words Brain macrophages ; DNA fragmentation ; Microglia ; Mitochondria ; Nigral cell death ; TUNEL technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apoptosis has been postulated as a mechanism of nerve cell death in Parkinson’s disease. In the present study, the substantia nigra of 22 neuropathologically confirmed Parkinson cases and 8 control brains was studied using the in situ end-labeling (TUNEL) method. About 50% of parkinsonian brains showed a small number of TUNEL-positive glial cells in the substantia nigra, whereas no neurons showed convincing TUNEL positivity or any morphological signs of apoptosis. No correlation was observed between the number of TUNEL-positive glial cells and microglial activation. Our results fail to demonstrate apoptosis as a mechanism of cell death in Parkinson’s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050590
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  • 9
    Electronic Resource
    Electronic Resource
    Low prevalence of apolipoprotein E ε4 allele in the neurofibrillary tangle predominant form of senile dementia (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 403-409 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Neurofibrillary ; tangle-predominant dementia ; Apolipoprotein E ; Amyloid ; Senile plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (apoE) genotypes were analyzed in a subset of demented very old patients who share a uniform neuropathological picture consisting of various numbers of neurofibrillary tangles (NFT) in allocortical areas of the inferomedial temporal lobe without significant numbers of either diffuse amyloid or neuritic plaques. Among 18 patients with this condition referred to as NFT-predominant senile dementia (average age at death 87 ± 4.7 years), we found allele frequencies of 0.11 ɛ2, 0.86 ɛ3 and 0.03 ɛ4, which are significantly different from allele frequencies reported in Alzheimer’s disease (0.04 ɛ2, 0.59 ɛ3 and 0.38 ɛ4). The low prevalence of the apoE ɛ4 allele in this subset of patients is striking and suggests that NFT-predominant senile dementia is a dementing neurodegenerative disease in which the deposition of Aβ-amyloid did not occur, possibly due to protective effects of ɛ2 and/or ɛ3 alleles or lack of a promoting effect of apoE ɛ4 on amyloidogenesis. We propose that NFT-predominant dementia is a variant of Alzheimer’s disease occurring in the very old.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050726
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  • 10
    Electronic Resource
    Electronic Resource
    Immuno gold staining (IGS) for electron microscopical demonstration of glial fibrillary acidic (GFA) protein in LR White embedded tissue (1985)
    Springer
    Histochemistry and cell biology 83 (1985), S. 497-500 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Post-embedding immunocytochemical staining methods using gold have so far failed to label intermediate filament antigens in situ in epon or araldite embedded tisue. We have now applied the post-embedding immuno gold staining (IGS) technique for LR White embedded tissue. Glial fibrillary acidic (GFA) protein immunoreactivity was clearly demonstrated electron microscopically on astrocytie filaments of rat cerebellum in situ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00492450
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