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  • 1
    Electronic Resource
    Electronic Resource
    Expression of vimentin, glial filament, and neurofilament proteins in primitive childhood brain tumors (1985)
    Springer
    Acta neuropathologica 68 (1985), S. 239-244 
    Details
    ISSN: 1432-0533
    Keywords: Intermediate filaments ; Medulloblastoma ; Immunohistochemistry ; Immunoblotting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two methods of determining intermediate filament protein (IFP) expression by primitive brain tumors of childhood were compared using a panel of monoclonal antibodies to three classes of IFP. In addition to a controlled immunohistochemical study, a group of these tumors was subjected to direct immunologic assay of tumor-extracted IFP using the western blot method. Western blots of IFP extracted from ten prospectively microdissected brain tumors revealed no NF200 or NF150 in any tumor. Traces of NF68, VFP, and GFP were detected by this sensitive method in four, three, and six cases, respectively. Immunohistochemistry, using the same monoclonal antibodies on adjacent tumor sections, yielded results significantly different from the immunoblotting method: no NF proteins or VFP were detected, but immunoreactive GFP could be seen in a small percentage of cells in each case. A retrospective study of 46 primitive tumors, using only immunohistochemistry, showed GFP to be the most common source of immunopositivity (38 cases), followed by VFP (15 cases), but most positive cells were judged to be reactive astrocytes. NF protein was not detected except in three cases in which extremely rare cells had morphological features of neurons. Cells which were clearly malignant, and which constituted the majority of cells in a microscopic field, were devoid of any IFP immunoreactivity. The advantages and limitations of each method of IFP detection in this group of primitive tumors and the implications of the apparent paucity of mature neural IFP in these tumors are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690201
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  • 2
    Electronic Resource
    Electronic Resource
    Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 269-276 
    Details
    ISSN: 1432-0533
    Keywords: Diffuse Lewy Body Disease ; Hippocampus ; Neurites ; Neurofilament ; Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ubiquitin-immunoreactive dystrophic neurites in the CA2/3 region of the hippocampus are characteristic of diffuse Lewy body disease (DLBD). The origin of dystrophic CA2/3 neurites is unknown, but their extent correlates with the number of cortical Lewy bodies (LBs). To examine the molecular composition of these lesions, hippocampal sections were obtained at postmortem from cases of DLBD, Parkinson's disease and Alzheimer's disease. The tissue samples were fixed in a variety of fixatives and immunostained with antibodies to ubiquitin, ubiquitin C-terminal hydrolase (PGP9.5), neurofilament protein subunits, tau protein, paired helical filaments and tyrosine hydroxylase (TH). In addition to being ubiquitin positive, both cortical LBs and CA2/3 dystrophic neurites were positive with a neurofilament monoclonal antibody (RM032) and PGP9.5; however, fewer lesions were detected with these antibodies compared to ubiquitin immunocyto-chemistry. The dystrophic CA2/3 neurites were not stained with antibodies to tau proteins, paired helical filaments or TH. Absence of TH immunoreactivity suggests that CA2/3 neuritic processes are not derived from brain stem dopaminergic afferents to the hippocampus. Since CA2/3 neurites are immunologically similar to cortical LB, the pathogenesis of these lesions may be similar. Characterization of dystrophic CA2/3 neurites and cortical LBs may clarify how these lesions contribute to the emergence of dementia in DLBD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296742
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  • 3
    Electronic Resource
    Electronic Resource
    Anti-neurofilament monoclonal antibodies: Reagents for the evaluation of human neoplasms (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 155-158 
    Details
    ISSN: 1432-0533
    Keywords: Neurofilaments ; Human neoplasms ; Monoclonal antibodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sixty human nervous system neoplasms were examined by immunohistochemistry using a monoclonal antibody against neurofilament triplet proteins. Only those of neuronal origin had tumor cells with intracytoplasmic, immunoreactive neurofilament triplet proteins. However, not all such neoplasms contained labeled tumor cells. Benign or differentiated neuronal tumors more often contained labeled cells than malignant, less differentiated neoplasms of the neuron series. We conclude that anti-neurofilament monoclonal antibodies are useful reagents for the evaluation of human neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691603
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  • 4
    Electronic Resource
    Electronic Resource
    Regulation of Tau Phosphorylation in Alzheimer's Disease (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 777 (1996), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Alzheimer's disease (AD) is a heterogeneous dementing disorder of the elderly that is characterized by progressive cognitive impairments and the accumulation of abundant amyloid or senile plaques (SPs) and neurofibrillary tangles (NFTs) as well as the massive loss of neutrons in the AD brain. Indeed, a secure diagnosis of AD in patients with a chronic progressive dementia requires evidence of numerous SPs and NFTs in the postmortem brain. Although the deposition of fibrillar amyloid or Aβ-peptides in extracellular plaques and the accumulation of tau-rich intraneuronal NFTs are not restricted exclusively to AD, there is a close correlation between the burden of tau-rich neurofibrillary lesions in selected telencephalic regions of the brain and the dementia in AD. Since the formation of neurofibrillary lesions from hyperphosphorylated tau proteins may compromise the function and viability of neurons in the AD brain, this review summarizes recent insights into mechanisms that regulate the phosphorylation state of tau in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb34408.x
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  • 5
    Electronic Resource
    Electronic Resource
    Monoclonal Antibodies to Gel-Excised Glial Filament Protein and Their Reactivities with Other Intermediate Filament Proteins (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 42 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A series of 14 monoclonal antibodies (MAs) has been obtained from a single rat-mouse fusion using gel-excised bovine glial filament (GF) proteins as immunogens. These MAs were characterized by two separate immunochemical assays and by two different immunohistochemical methods. Nine MAs demonstrated specificity for GF proteins. One MA also recognized an epitope shared by intermediate filaments (IF) of the vimentin class (VF). Using the enzyme-linked immunosorbent assay, four of the MAs recognized 200,000, 150,000, and 51,000 dalton proteins, suggesting that these MAs were specific for GF proteins (the 51,000 dalton protein) and neurofilament (NF) proteins (the two high-molecular-weight proteins). However, in both of the immunohistochemical assay systems, these MAs stained neurons and their processes but not astroglial cells. These observations strongly suggest that the 51,000–dalton protein recognized by these four MAs was not derived from GF proteins but instead represents derivatives of NF protein subunits comigrating in gels with GF proteins. These data provide additional information concerning the unique and shared antigenic determinants of the three classes of IF (NF, GF, and VF) of the CNS. In addition, they draw attention to the fact that proteins of certain IF may undergo degradation and comigrate in gels with the proteins of unrelated IF. This emphasizes the need for the use of independent immunochemical and immunohistochemical assays in the characterization of the specificity of MAs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb09692.x
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  • 6
    Electronic Resource
    Electronic Resource
    An Immunoblot Study of Neurofilament Degradation In Situ and During Calcium-Activated Proteolysis (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 44 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The degradation of neurofilament (NF) proteins was examined by immunoblot methods to identify, characterize, and monitor the appearance of immunoreactive breakdown products during the loss of NF triplet proteins. Individual NF proteins and their breakdown products were identified using polyclonal and monoclonal antibodies to NF proteins. NF degradation was compared during calcium-activated proteolysis of isolated rat NF, during an experimental influx of calcium into excised rat spinal nerve roots, and during NF breakdown in transected rat peripheral nerve. These different experimental conditions produced similar patterns of NF fragmentation, including the transient appearance of NF immunobands between Mr 150,000–200,000 and 110,000–120,000 as well as the appearance and accumulation of NF immunobands between Mr 45,000 and 65,000. Most immunoreactive NF fragments remained Triton-insoluble. Low levels of the same immunoreactive fragments were present in control neural tissues, suggesting that calciumactivated proteolysis may be operative in the turnover and/or processing of NF proteins in vivo. Very similar patterns of NF degradation during experimental calcium influxes into different CNS and PNS tissues are indicative of the widespread distribution of calcium-activated NF protease in neural tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb05442.x
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  • 7
    Electronic Resource
    Electronic Resource
    Persistence of Immunoreactive Neurofilament Protein Breakdown Products in Transected Rat Sciatic Nerve (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 43 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Alterations occurring in nerve proteins of transected nerves were studied in rat sciatic nerves using polyclonal and monoclonal antibodies to identify and monitor neurofilament (NF) epitopes among nerve proteins following their electrophoresis and transfer to nitrocellulose paper. Immunoblot methods identified NF epitopes in NF triplet proteins (Mr 200,000, 150,000, and 68,000) and in NF nontriplet proteins (all other immunobands below Mr 200,000 and above Mr 40,000). NF triplet and nontriplet proteins were Triton-insoluble in both untransected and transected nerves. Extensive loss of NF triplet and most nontriplet proteins occurred during the 24-48-h period following nerve transection and was attributed to proteolytic degradation. Loss of protease-labile NF proteins led to a markedly reduced level of NF immunoreactivity in 2-day transected nerve. NF proteins which survived the 2-day posttransectional period were considered to represent protease-stable NF fragments. These fragments persisted in transected nerve for periods of at least 35 days. Most protease-stable NF fragments which retained immunoreactivity had Mr of 57,000-65,000. Low concentrations of the same immunobands were present in untransected nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb12809.x
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  • 8
    Electronic Resource
    Electronic Resource
    Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 269-276 
    Details
    ISSN: 1432-0533
    Keywords: Key words: Diffuse Lewy Body Disease – Hippocampus – Neurites – Neurofilament – Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Ubiquitin-immunoreactive dystrophic neurites in the CA2/3 region of the hippocampus are characteristic of diffuse Lewy body disease (DLBD). The origin of dystrophic CA2/3 neurites is unknown, but their extent correlates with the number of cortical Lewy bodies (LBs). To examine the molecular composition of these lesions, hippocampal sections were obtained at postmortem from cases of DLBD, Parkinson's disease and Alzheimer's disease. The tissue samples were fixed in a variety of fixatives and immunostained with antibodies to ubiquitin, ubiquitin C-terminal hydrolase (PGP9.5), neurofilament protein subunits, tau protein, paired helical filaments and tyrosine hydroxylase (TH). In addition to being ubiquitin positive, both cortical LBs and CA2/3 dystrophic neurites were positive with a neurofilament monoclonal antibody (RM032) and PGP9.5; however, fewer lesions were detected with these antibodies compared to ubiquitin immunocytochemistry. The dystrophic CA2/3 neurites were not stained with antibodies to tau proteins, paired helical filaments or TH. Absence of TH immunoreactivity suggests that CA2/3 neuritic processes are not derived from brain stem dopaminergic afferents to the hippocampus. Since CA2/3 neurites are immunologically similar to cortical LB, the pathogenesis of these lesions may be similar. Characterization of dystrophic CA2/3 neurites and cortical LBs may clarify how these lesions contribute to the emergence of dementia in DLBD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296742
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  • 9
    Electronic Resource
    Electronic Resource
    Association of apolipoprotein ɛ4 allele and neuropathologic findings in patients with dementia (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 239-243 
    Details
    ISSN: 1432-0533
    Keywords: Apolipoprotein E ; Dementia ; Diffuse Lewy body disease ; Alzheimer's disease ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (APOE) is a lipoprotein expressed in liver and brain as one of three isoforms (APOE 2, APOE 3 and APOE 4). Recent findings suggest that the presence of APOE 4 is associated with an increased risk for both familial Alzheimer's disease and late-onset Alzheimer's disease. We extended these observations by determining the frequency of APOE alleles in patients with pathologically confirmed Alzheimer's Disease (AD), Parkinson's disease (PD), diffuse Lewy Body disease (DLBD), AD with concomitant PD pathology, demented PD patients without or with concomitant AD pathology and in schizophrenics with a progressive dementia (SCHIZ+DEM). The APOE genotype was determined by restriction digestion of polymerase chain reaction-amplified DNA isolated from frozen brain samples. The frequency of the APOE ɛ4 allele was highest among sporadic AD and DLBD patients (0.30 and 0.38, respectively) and lowest in the SCHIZ+DEM and non-demented PD patients (0.06 and 0.1, respectively). Thus, the APOE ɛ4 allele is over-represented selectively in patients with dementias associated with plaques and tangles and/or cortical Lewy bodies, but not in demented schizophrenics or non-demented PD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296506
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  • 10
    Electronic Resource
    Electronic Resource
    Association of apolipoprotein ε4 allele and neuropathologic findings in patients with dementia (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 239-243 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E ; Dementia ; Diffuse Lewy body disease ; Alzheimer's disease ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (APOE) is a lipoprotein expressed in liver and brain as one of three isoforms (APOE 2, APOE 3 and APOE 4). Recent findings suggest that the presence of APOE 4 is associated with an increased risk for both familial Alzheimer's disease and late-onset Alzheimer's disease. We extended these observations by determining the frequency of APOE alleles in patients with pathologically confirmed Alzheimer's Disease (AD), Parkinson's disease (PD), diffuse Lewy Body disease (DLBD), AD with concomitant PD pathology, demented PD patients without or with concomitant AD pathology and in schizophrenics with a progressive dementia (SCHIZ+DEM). The APOE genotype was determined by restriction digestion of polymerase chain reaction-amplified DNA isolated from frozen brain samples. The frequency of the APOE ε4 allele was highest among sporadic AD and DLBD patients (0.30 and 0.38, respectively) and lowest in the SCHIZ+DEM and non-demented PD patients (0.06 and 0.1, respectively). Thus, the APOE ε4 allele is over-represented selectively in patients with dementias associated with plaques and tangles and/or cortical Lewy bodies, but not in demented schizophrenics or non-demented PD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296506
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