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  • 1
    Electronic Resource
    Electronic Resource
    Immunoreactivity of CD45, a protein phosphotyrosine phosphatase, in Alzheimer's disease (1991)
    Springer
    Acta neuropathologica 83 (1991), S. 12-20 
    Details
    ISSN: 1432-0533
    Keywords: CD45 ; Protein phosphotyrosine phosphatase ; Microglia ; Intracellular signaling ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both protein kinases and phosphoprotein phosphatases are important components of signal transduction systems in cells. Recent studies in Alzheimer's disease (AD) have shown abnormal protein phosphorylation in the cortex suggesting an alteration in these enzymes. In the present study, an antibody against CD45 was used to analyze the status of this protein phosphotyrosine phosphatase in AD. We studied and quantified the immunohistochemical and immunochemical distribution of this integral membrane protein in control and AD brain. We found that anti-CD45 immunostained the great majority of microglia, both resting and activated. These cells were Ricinus communis agglutinin I positive and glial fibrillary acidic protein and neurofilament negative. The AD frontal cortex showed a 35% (P〈0.01) increase in the number of anti-CD45 immunoreactive microglia as compared with controls. These results were consistent with the immunoblot quantification of CD45 immunoreactivity following native gel electrophoresis. In AD, 30% of the CD45-immunostained microglia were clustered in the neuritic plaques (about six per plaque) while the remaining 70% were scattered in the neuropil. The AD hippocampus showed an increase in CD45-immunoreactive microglia in the molecular layer of the dentte gyrus. At the ultrastructural level, CD45 immunoreactivity was localized exclusively to the plasma membrane of the microglia. The presence of the anti-CD45 immunoreactivity in microglia suggests the possibility that they may require the presence of CD45 as a cell surface receptor which may regulate cell function through modulation of intracellular signaling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294425
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  • 2
    Electronic Resource
    Electronic Resource
    A neuropathological subset of Alzheimer's disease with concomitant Lewy body disease and spongiform change (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 194-201 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer disease ; Diffuse Lewy body disease ; Spongiform change ; Creutzfeldt-Jakob disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The neuropathological heterogeneity of Alzheimer's disease (AD) is increasingly recognized. Diffuse Lewy body disease, for example, most frequently occurs in cases fulfilling histopathological criteria for AD, and these patients usually present with dementia rather than parkinsonism. We report five cases of concomitant AD and diffuse Lewy body disease with still another coexistent neuropathological feature: localized and stereotyped spongiform change in the neuropil. This spongiform change was most striking in the superior and inferior temporal, entorhinal, and insular cortex and the amygdala and was virtually indistinguishable from that seen in Creutzfeldt-Jakob disease. Electron microscopic study on one case revealed membrane-containing vacuoles in close association with neuritic plaques and plaired helical filament-filled processes. Immunocytochemistry using antibodies to prion proteins (PrPsc or PrP27–30) failed to label plaque or vascular amyloid in the five cases. Four primates inoculated with brain tissue from one case have not evidenced neurological disease in the 3 years since the transmission experiment. We conclude that these cases represent a neuropathological subset of AD with relatively widespread Lewy bodies and a localized spongiform change, predominantly involving the medial temporal region. Despite the light and electron microscopic commonality with Creutzfeldt-Jakob disease, there is no clear evidence that these cases represent a form of transmissible spongiform encephalopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688209
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  • 3
    Electronic Resource
    Electronic Resource
    Lobar atrophy with dense-core (brain stem type) Lewy bodies in a patient with dementia (1990)
    Springer
    Acta neuropathologica 80 (1990), S. 453-458 
    Details
    ISSN: 1432-0533
    Keywords: Dementia ; Neuronal inclusions ; Pick's disease ; Lewy bodies ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 62-year-old man presented with memory impairment progressing over 6 years to dementia with near mutism and was diagnosed as having Alzheimer's disease. At autopsy his brain showed lobar atrophy suggestive of Pick's disease and there were spherical intracytoplasmic neuronal inclusions in the fascia dentata, hippocampal pyramidal cell layer, and temporal cortex. Unlike Pick bodies, however, the inclusions were eosinophilic with H&E stains, non-argyrophilic, and failed to react immunohistochemically with antibodies to paired helical filaments or Alz-50. They did label with antibodies to ubiquitin, however, and electron microscopy disclosed dense-cored granular structures with thin filamentous coronas which resembled brain stem-type Lewy bodies. The substantia nigra and locus coeruleus were not affected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307702
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  • 4
    Electronic Resource
    Electronic Resource
    Immunoelectron microscopic study of synaptic pathology in Alzheimer's disease (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 428-433 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Biopsy ; Synapses ; Synaptophysin ; Immunoelectron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Alzheimer's disease (AD) is characterized by an extensive loss of neurons and synapses in the neocortex which correlates strongly with psychometric tests of dementia. To characterize the ultrastructural changes in presynaptic terminals in AD, we studied biopsy material from the frontal cortex. We also examined, at the ultrastructural level, abnormal neurites scattered in the AD neuropil and in the plaque region using sections from autopsy material immunolabeled with anti-synaptophysin. We found that, regardless of amyloid deposits, some presynaptic terminals were distended and contained swollen vesicles and dense bodies. These altered synaptic organelles were similar to those found in dystrophic neurites. The latter structures displayed synaptophysin immunoreactivity, mostly localized to outer membranes of synaptic vesicles and dense bodies. The present study supports the hypothesis of progressive synaptic pathology in AD neocortex and favors the notion that the dystrophic process originates from presynaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293464
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  • 5
    Electronic Resource
    Electronic Resource
    Neurotrophic and Neuroprotective Effects of hAPP in Transgenic Mice (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: To better understand the role the human amyloid precursor protein (hAPP) plays in Alzheimer's disease (AD), it is essential to define its primary function(s). Here we expressed different hAPPs in neurons of transgenic (tg) mice to characterize their effects on the intact central nervous system (CNS). Immunolabeled brain sections of tg and non-tg mice were compared quantitatively by microdensitometry and computer-aided analysis of laser scanning confocal digitized images. Compared with non-tg mice, tg mice overexpressing hAPPs showed an increase in the number of synaptophysin immunoreactive presynaptic terminals as well as in the expression of the growth-associated marker GAP-43. While non-tg controls and tg mice expressing hAPP751 at moderate levels displayed a normal pattern of reinnervation of the dentate gyrus following perforant pathway transection, tg mice expressing hAPP695 at severalfold higher levels showed an accentuation of the synaptic loss and no sprouting reaction. In addition, expression of hAPP751 at moderate levels effectively protected neurons against excitotoxic injury induced either acutely by systemic injection of kainic acid or chronically by transgene-driven glial production of the soluble HIV-1 protein gp120. Neuronal expression of hAPP695 at higher levels provided less excitoprotection. Our findings are consistent with the postulate that APP plays a role in the formation/maintenance of synapses and that processes which affect this function could contribute to the synaptic pathology seen in AD. Our study also revealed that hAPPs can exert important excitoprotective functions in vivo and that the efficiency of this protection may depend on the hAPP isoform expressed as well as on the level of neuronal hAPP expression. Neuronal overexpression of hAPP beyond a certain level may have detrimental effects on the CNS, particularly in the context of secondary neural injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb34405.x
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  • 6
    Electronic Resource
    Electronic Resource
    Morphological, Biochemical, and Genetic Support for an Apolipoprotein E Effect on Microtubular Metabolism (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: There are two distinct viewpoints on the association of the inheritance of apolipoprotein E (APOE) alleles and the age of onset distribution of Alzheimer's disease (AD): genetic and phenotypic expression. There have been multiple corroborations of the APOE-ε4 association with Alzheimer's disease in populations around the world in clinic based studies as well as emerging epidemiological studies. The genetic data do not imply mechanism of pathogenesis. The phenotypic expression of AD has been based in theories based on amyloid plaques or neurofibrillary tangles. ApoE protein interacts with both β-amyloid and tau in an isoform-specific manner. The interaction with tau had been thought to be an in vitro artifact, since apoE had not been previously localized to the
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb34413.x
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  • 7
    Electronic Resource
    Electronic Resource
    Altered Protein Tyrosine Phosphorylation in Alzheimer's Disease (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The activity of protein tyrosine kinases was determined in extracts from Alzheimer's disease brains and age-and postmortem time-matched control brains at autopsy using the synthetic peptide substrate poly(Glu4Tyr1). The specific activity of protein tyrosine kinases in the particulate fraction decreased roughly twofold (p 〈 0.02) in Alzheimer's disease frontal cortex relative to unaffected control cortex. Cytosolic protein tyrosine kinase activity in Alzheimer's disease tissue was not significantly different from that in control tissue. In contrast to reduced particulate protein tyrosine kinase activity, analysis of Western blots of cytosolic and particulate fractions revealed increases in cytosolic antiphosphotyrosine immunoreactive polypeptides with molecular masses of 55 and 60 kDa. Quantitative immunohistochemistry and morphometry of frontal cortex sections with the antiphosphotyrosine antibody indicated increased antiphosphotyrosine staining in the neurons, although the number of antiphosphotyrosine-positive neurons per square millimeter decreased. Also, increased antiphosphotyrosine staining was observed in the hippocampal neurons. These results suggest that altered protein tyrosine kinases and protein tyrosine phosphorylation are involved in the pathology of Alzheimer's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb11405.x
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  • 8
    Electronic Resource
    Electronic Resource
    Correlation of nicotinic binding with neurochemical markers in Alzheimer's disease (1998)
    Springer
    Journal of neural transmission 105 (1998), S. 709-717 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Nicotinic receptor ; binding ; Alzheimer's disease.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The loss of neocortical synapses that occurs in Alzheimer's disease (AD) has been shown to correlate with cognitive decline. In addition, marked losses in the cholinergic system in AD, specifically choline acetyltransferase (ChAT) activity and high affinity presynaptic neuronal nicotinic cholinergic receptors (nAChRs), have also been described. We hypothesized that in AD, the loss of [3H]-ligand binding to nAChRs, which are largely presynaptic, would correlate with changes in two other presynaptic markers: synaptophysin (Syn), a measure of synaptic density, and ChAT activity. The midfrontal (MF) cortex of 36 autopsy confirmed (NIA and CERAD criteria) AD patients (mean death age ± SD 80.1 ± 8.4 years) who met NINDS-ADRDA criteria for a clinical diagnosis of probable or possible AD, and 11 nondemented controls (mean death age ± SD 77.9 ± 8.0) were examined. Synapse counts were quantified by a dotimmunobinding assay for Syn. ChAT activity was assessed by standard biochemical assays. Nicotinic cholinergic receptor binding was assayed using the high affinity nicotinic agonist [3H]- (±)-epibatidine ([3H]-EPI). The mean ± SD Syn in AD (83.4 ± 31.9 arbitrary units (AU)/mg protein) was significantly lower than controls (126.1 ± 19.9, p = 0.0003; t-test). The mean ChAT activity in AD (139.0 ± 75.6 nmol ACh/hr/100 mg protein) was significantly lower than controls (219.6 ± 70.8, p = 0.004). The mean [3H]-EPI total binding in AD (6.2 ± 2.8 fmol/mg protein) was significantly lower than controls (14.8 ± 3.2; p 〈 0.0001). Syn correlated with [3H]-EPI binding in AD (r = 0.48, p = 0.006; Pearson) but ChAT did not (r = −0.20, p = 0.34). We conclude that loss of high affinity nAChR binding correlates with loss of synapses in AD. The lack of correlation between [3H]-EPI binding and ChAT activity suggests that the targeted receptor populations may not be located exclusively on cholinergic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050090
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  • 9
    Electronic Resource
    Electronic Resource
    Neurofibrillary tangles in the dentate granule cells of patients with Alzheimer’s disease, Lewy body disease and progressive supranuclear palsy (1996)
    Springer
    Acta neuropathologica 93 (1996), S. 7-12 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neurofibrillary tangle ; Dentate granule cell ; Alzheimer’s disease ; Lewy body disease ; Progressive ; supranuclear palsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have shown that the dentate granular cells of the hippocampus are affected in patients with Alzheimer’s disease (AD). To gain a better understanding of the cytoskeletal alterations in these cells, we carried out immunocytochemical and immunoelectron microscopic analysis of the dentate gyrus of patients with primary degenerative dementias, using a monoclonal antibody against paired helical filaments (TG3). This antibody labeled a large number of spherical inclusions in the dentate granule cells of patients with AD and its Lewy body variant (LBV). These inclusions consisted of straight tubular structures (about 18–25 nm in diameter), similar to those found in progressive supranuclear palsy (PSP). These inclusions, although in a smaller number, were also found in demented patients with PSP, but not in those with diffuse Lewy body disease or age-matched controls. These findings indicate that the neurofibrillary alterations in the dentate granule cells of patients with AD, LBV and PSP share cytoskeletal similarities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050576
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  • 10
    Electronic Resource
    Electronic Resource
    Alterations in glutamate receptor 2/3 subunits and amyloid precursor protein expression during the course of Alzheimer’s disease and Lewy body variant (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 539-548 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Lewy body variant ; Glutamate receptor ; Amyloid precursor protein ; expression ; Vulnerability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations in the processing and patterns of trophic and/or toxic factors might lead to the increased neuronal vulnerability in the entorhinal cortex in Alzheimer’s disease (AD) and Lewy body variant (LBV). Therefore, patterns and levels of amyloid precursor protein (APP) and glutamate receptor (gluR) expression in the entorhinal cortex and hippocampus in relation to disease severity were investigated. Sections from the hippocampus and entorhinal cortex were single and double immunolabeled for APP, gluR2/3, and n-methyl-d-aspartate receptor (NMDA-R). Within the hippocampus and entorhinal cortex, image analysis revealed progressively decreased APP and gluR2/3 levels during the course of AD and LBV, whereas levels of NMDA-R were unaltered. Furthermore, the present study showed a positive correlation and close co-localization of APP and gluR2/3 immunoreactivity in neurons, suggesting a possible interaction between these two factors. In conclusion, these data imply that alterations in neuronal APP and gluR2/3 expression in the entorhinal cortex lead to increased susceptibility to neurodegeneration and might be markers of vulnerability.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050748
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