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  • 1
    Electronic Resource
    Electronic Resource
    Expression of the histocompatibility glycoprotein HLA-DR in neurological disease (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 550-557 
    Details
    ISSN: 1432-0533
    Keywords: HLA-DR ; Reactive microglia ; Macrophages ; Astrocytes ; Neuropathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reactive microglia or macrophages expressing the histocompatibility glycoprotein HLA-DR were detected in many neurological diseases including Alzheimer's, Parkinson's, Pick's and Huntington's diseases, parkinsonism-dementia of Guam, amyotrophic lateral sclerosis, Shy-Drager syndrome, multiple sclerosis and AIDS encephalopathy. Reactive astrocytes, also present in these conditions, were established as a population distinct from the HLA-DR positive microglia by double immunostaining for glial fibrillary acidic protein and HLA-DR. A distinctive pattern of HLA-DR positive cells was seen in each disease entity. Areas known to contain pathology always stained positively, and, in several cases, reactive microglia appeared in areas that would otherwise not have been suspected of being involved in the pathological process. HLA-DR staining, which outlines the surface membranes of positive cells, was so strong that lesioned areas could frequently be identified in sections with the naked eye. In adjacent sections stained with H&E or sections destained of HLA-DR and then restained with H&E, gliosis was often hard to identify except on close microscopic inspection. The results suggest that HLA-DR staining may be a valuable addition to standard neuropathological methods and might be useful in investigating diseases where pathology has not yet been identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689592
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  • 2
    Electronic Resource
    Electronic Resource
    Senile plaques, amyloid β-protein, and acetylcholinesterase fibres: laminar distributions in Alzheimer's disease striate cortex (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 292-299 
    Details
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Visual cortex ; Amyloid ; Acetylcholinesterase ; Histopathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The laminar distributions of senile plaques and amyloid β-protein (AβP) within the striate cortex of patients with Alzheimer's disease (AD) were studied with enhanced Bielschowsky (roughly equivalent to the Campbell technique) and immunohistochemical methods. The laminar distribution of acetylcholinesterase (AChE) fibres within the striate cortex of both AD patients and control patients was studied with an enzyme histochemical method. Quantification of Bielschowsky-stained plaque numbers along intersect lines drawn parallel to laminar boundaries revealed a significant aggregation of plaques at the interface of layers IVc and V. Lines drawn through layer VI intersected significantly fewer plaques than lines through other laminae. Immunoperoxidase staining for AβP revealed a similar distribution fo senile plaques, and additional, prominent, diffuse deposits of AβP within layers I and IVc. AChE fibres were markedly depleted in the striate cortex of AD cases. In control cases, AChE fibres were, like AβP immunoreactivity, concentrated within layers I and IVc. The results indicate that enhanced silver methods may not reveal the complete distribution of AβP. The codistribution of AβP-immunoreactive diffuse amyloid deposits and AChE fibres to the same cortical laminae is consistent with the possibility that these deposits may be formed from degenerating cholinergic elements. The formation of a line of senile plaques at the interface of two cortical laminae within the striate cortex, in an anatomically analogous situation to a similar line of plaques within the dentate gyrus, suggests that formation of well-defined plaques may be accelerated by the interaction of specific neuronal systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296792
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  • 3
    Electronic Resource
    Electronic Resource
    Loss of insulin receptor immunoreactivity from the substantia nigra pars compacta neurons in Parkinson's disease (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 343-348 
    Details
    ISSN: 1432-0533
    Keywords: Parkinson's disease ; Substantia nigra ; Insulin receptor ; Immunochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immunohistochemistry using both a newly developed polyclonal, and a commercially available monoclonal, anti-insulin receptor antibody was done on the midbrain from cases of idiopathic Parkinson's disease (PD), Alzheimer's disease, amyotrophic lateral sclerosis, vascular parkinsonism and non-neurological controls. Both antibodies gave indentical patterns of neuronal staining. The neurons of the oculomotor nucleus were immunopositive in all the brains. However, the neurons in the pars compacta of the substantia nigra, paranigral nucleus, parabrachial pigmental nucleus, tegmental pedunculopontine nucleus, supratrocheal nucleus, cuneiform nucleus, subcuneiform nucleus and lemniscus medialis, which were positive in other diseases and in non-neurological controls, were not stained by these antibodies in PD brains. These results suggest that, in PD, a dysfunction of the insulin/insulin receptor system may precede death of the dopaminergic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00313602
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  • 4
    Electronic Resource
    Electronic Resource
    Lewy bodies in Parkinson's disease are recognized by antibodies to complement proteins (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 100-104 
    Details
    ISSN: 1432-0533
    Keywords: Parkinson's disease ; Complement ; Lewy bodies ; Oligodendrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The substantia nigra (SN) in 11 Parkinson's disease (PD) patients and 5 neurologically normal controls was examined immunohistochemically using antibodies to various proteins of the complement system. In PD, but not in control SN, intra-and extraneuronal Lewy bodies and dendritic spheroid bodies were stained with anti-human C3d, C4d, C7 and C9 antibodies, but not with antibodies to C1q, fraction Bb of factor B or properdin. Axonal spheroid bodies in the nigrostriatal tract were not stained by any of the complement antibodies. However, complement-activated oligodendroglia were revealed by anti-C3d and anti-C4d antibodies in the PD substantia nigral area. These data indicate that some pathological structures in PD activate the classical complement pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427222
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  • 5
    Electronic Resource
    Electronic Resource
    Further observations on Tau-positive glia in the brains with progressive supranuclear palsy (1993)
    Springer
    Acta neuropathologica 85 (1993), S. 308-315 
    Details
    ISSN: 1432-0533
    Keywords: Progressive supranuclear palsy ; Astrocyte ; Alzheimer type I glia ; CD44 ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The previously reported unusual, Tau-positive glia with astrocytic morphology seen in brain tissues from cases of progressive supranuclear palsy (PSP) were re-examined immunohistochemically using antibodies to CD44 and vimentin, as well as Alz-50. Four brains of PSP cases, one of whom had atypical clinical features, were examined. All four cases showed the unusual glia which were positive to Alz-50 and anti-CD44 antibodies, but negative to anti-vimentin antibody. Ultrastructurally, they had either paired nucleated or lobulated nuclei and the cytoplasm frequently contained lipofuscin pigment. The CD44 was located on the surface of the cell bodies and their processes. Such glia were most numerous in the striatum in all cases. They also appeared in the cortex and some subcortical nuclei in the three typical cases. They were not seen in the lower brain stem or cerebellum. In their morphological characteristics and regionally specific appearance, these unusual glia seemed similar to the Alzheimer type I glia which are commonly seen in hepatic encephalopathy or Wilson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227727
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  • 6
    Electronic Resource
    Electronic Resource
    THE INHIBITORY ACTION OF 3-HYDROXYTYRAMINE, GAMMA-AMINOBUTYRIC ACID (GABA) AND SOME OTHER COMPOUNDS TOWARDS THE CRAYFISH STRETCH RECEPTOR NEURON (1961)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 8 (1961), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1961.tb13524.x
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  • 7
    Electronic Resource
    Electronic Resource
    Anti-Inflammatory Drugs in the Fight against 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: Lesions in Alzheimer disease are characterized by the assembly of a variety of cells and proteins associated with the immune system. Activated microglia express high levels of MHC glycoproteins and receptors for complement. Small numbers of T-lymphocytes infiltrate tissue. Proteins of the classical complement pathway are closely connected with β-amyloid deposits. Several materials associated with senile plaques, including β-amyloid protein itself, bind C1q in vitro and activate the pathway. The membrane attack complex of complement, as well as proteins which defend against that complex, colocalize with dystrophic neurites. These data imply that an autodestructive process is occurring in Alzheimer's disease, and that anti-inflammatory drugs might be an effective form of therapy. Some epidemiological evidence and results of a pilot clinical trial support this hypothesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb34421.x
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibitory Properties of the Catecholamines (1961)
    [s.l.] : Nature Publishing Group
    Nature 192 (1961), S. 563-563 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Pacifastacus leniusculus (Dana) was the crayfish used and the method was essentially that described by Florey1 and by Elliott and Florey5. The commercially obtained compounds were made up in 'crayfish saline'6 at pH. 6-5-7 and the 'threshold blocking concentration' was determined; this was the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/192563a0
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  • 9
    Electronic Resource
    Electronic Resource
    Chemistry of Mood and Emotion (1980)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Psychology 31 (1980), S. 273-307 
    Details
    ISSN: 0066-4308
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Psychology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.ps.31.020180.001421
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  • 10
    Electronic Resource
    Electronic Resource
    Changes in Muscarinic Binding in Distant Brain Regions Showing Neuronal Losses After Folic Acid Injections into the Substantia Innominata (1983)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 40 (1983), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Injection of folic acid (FA) into the nucleus substantia innominata (NSI) was found to decrease [3H]quinuclidinyl benzilate ([3H]QNB) binding in the frontal cortex, pyriform cortex, amygdala, and the NSI itself without changing the Kd. Binding in the thalamus, caudate nucleus, hippocampus, and substantia nigra was not affected. [3H]Flunitrazepam binding was unchanged in all eight regions studied. Previous work indicates FA injections into the NSI produce epileptiform activity and cause loss of GABAergic and possibly other neurons in the frontal and pyriform cortices, the amygdala, and thalamus. The reductions of [3H]QNB binding in the first three of these regions are interpreted as indicating that many of the neurons lost are cholinoceptive, a finding that supports the previous hypothesis that activation of cholinergic projections from the NSI is an important part of the mechanism of cell loss in these regions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1983.tb08151.x
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