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  • 1
    Electronic Resource
    Electronic Resource
    Neurone loss in the nucleus basalis of meynert in Creutzfeldt-Jakob disease (1984)
    Springer
    Acta neuropathologica 65 (1984), S. 85-88 
    Details
    ISSN: 1432-0533
    Keywords: Nucleus basalis of Meynert ; Neuronal loss ; Creutzfeldt-Jakob disease ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a man of 47 with a 2-month history of Creutzfeldt-Jakob-disease verified neuropathologically a morphometric study of the nucleus basalis of Meynert, the major source of cholinergic innervation of the cortex, revealed a neuronal loss of 45%. The degeneration of these neurones may provide the morphological substrate of the cortical cholinergic deficiency which has been reported in this condition. The six subpopulations of the nucleus basalis were affected in different degrees. Neuronal loss was most pronounced in those subpopulations which project to cortical areas most affected by spongiosis and neuronal loss. It is suggested that maintenance of the nucleus basalis complex is a necessary condition for higher cortical function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689832
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  • 2
    Electronic Resource
    Electronic Resource
    Amyloid deposition in the nucleus basalis of Meynert complex: a topographic marker for degenerating cell clusters in Alzheimer's disease (1988)
    Springer
    Acta neuropathologica 75 (1988), S. 226-232 
    Details
    ISSN: 1432-0533
    Keywords: Nucleus basalis of Meynert ; Amyloid ; Neuronal loss ; Alzheimer's disease ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The deficiency of the cholinergic cortical projection system arising in the different basal forebrain structures collectively referred to as nucleus basalis of Meynert complex is a constant finding in Alzheimer's disease, a disorder which is neuropathologically characterised by the appearance of three intracerebral formes of twisted β-pleated sheet (amyloid) fibrils, neurofibrillary tangles, amyloid-containing neuritic plaques and congophilic amyloid angiopathy. In the present study the quantitative relationship between these hallmarks of the disease, amyloid deposition and neuronal loss in the cholinergic basal forebrain system, was investigated in ten cases of Alzheimer's disease. Besides a constant involvement of the cerebral cortex and hippocampus, all cases of Alzheimer's disease show a large amount of amyloid in the medial septal nucleus, in the diagonal band nucleus and in the substantia innominata which is correlated with neuronal loss in these areas. These amyloid deposits in the basal forebrain are due to congophilic angiopathy associated with plaques and neurofibrillary tangles. The distribution of amyloid deposition in the basal forebrain is restricted entirely to those neuronal clusters which represent the origin of cholinergic innervation of the cerebral cortex and hippocampus. Immediately adjacent structures are not affected. These findings suggest a pathogenetic role of amyloid deposition in the mechanism of degeneration of the cholingeric basal forebrain system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690530
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  • 3
    Electronic Resource
    Electronic Resource
    Abnormally phosphorylated protein tau in the cortex of aged individuals of various mammalian orders (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 305-312 
    Details
    ISSN: 1432-0533
    Keywords: Key words Aging ; Animal model ; Cortex ; Microtubule-associated protein tau ; Hyperphosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aged individuals of mammalian species displaying hyperphosphorylated tau protein may be suitable natural models for investigating neurodegenerative alterations occurring, for example, in Alzheimer’s disease. Therefore, autoptic tissue from the entorhinal, motor and prefrontal cortices of 14 mammalian species was screened using the monoclonal antibody AT8, which is directed against a phosphorylated epitope of human tau and applicable to the tissues of aged domestic animals, as shown in previous studies. AT8-immunoreactive neuronal processes and perikarya were revealed in Campbell’s guenon, rhesus monkey, baboon, rabbit, spectacled bear, guanaco, reindeer and bison. Signs for considerable neuropathological alterations in aged bisons also included neuropil threads, whereas AT8 immunoreactivity in the other species was only sparsely scattered. Hyperphosphorylated tau in the brain of an 28-year-old rhesus monkey was also detected by AT100, PHF-1 and TG-3 antibodies, but only in the hippocampal formation and entorhinal cortex, which are known as starting point for tangle spreading in the cortex of Alzheimer patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000183
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  • 4
    Electronic Resource
    Electronic Resource
    Loss of neurons in the nucleus basalis of Meynert in Alzheimer's disease, paralysis agitans and Korsakoff's disease (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 101-108 
    Details
    ISSN: 1432-0533
    Keywords: Nucleus basalis of Meynert ; Neuronal loss ; Dementia ; Alzheimer's disease ; Paralysis agitans ; Korsakoff's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The nucleus basalis of Meynert, the major source of cholinergic innervation of the cerebral cortex, was morphometrically investigated in 58 cases of neuropsychiatric disorders and compated to 14 controls. The results demonstrate a loss of neurons in the nucleus basalis of Meynert in Alzheimer's disease (70%), paralysis agitans (77%), and Korsakoff's disease (47%) but no marked reduction of neurons in postencephalitic parkinsonism, Huntington's disease, chronic alcoholism without dementia, schizophrenia and infantile brain damage. Neurons of the three subdivisions of the nucleus basalis of Meynert (the nucleus septi medialis, the nucleus of the diagonal band of Broca and the nucleus basalis Meynert neurons in the substantia innominata) may be affected in a different manner in different patients within a single group homogeneous with respect to the usual clinical and neuropathological diagnostic criteria. Cell loss in the basal forebrain is restricted to the large neurons of the nucleus basalis, the immediately adjacent neurons of the globus pallidus externus not being affected. The selective degeneration of these neurons provides the morphological correlate of the cortical cholinergic deficiency in these neuropathological conditions. The degeneration of this discrete cholinergic neuronal population in several disorders of higher cortical function is probably directly related to the progressive deterioration of memory and cognitive processes in affected patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00697388
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  • 5
    Electronic Resource
    Electronic Resource
    Cholinergic transmission in subcortical and cortical visual centers of rats: No evidence for the involvement of primary optic system (1977)
    Springer
    Experimental brain research 27 (1977), S. 211-219 
    Details
    ISSN: 1432-1106
    Keywords: Visual system ; Degeneration ; AChE ; Choline acetyltransferase ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of unilateral enucleation, ablation of the visual cortex or coagulation of the lateral geniculate nucleus (LGN) upon the activity of choline acetyltransferase (ChAc) and acetylcholinesterase (AChE) in different structures of the visual system of albino rats was studied. The localization and extent of the degeneration pattern were followed up by histological silver degeneration methods. Afferents from the retina project mainly contralaterally to the dorsal and ventral LGN, the pretectal region and the superior colliculus. Afferent fibres from the dorsal LGN enter the visual cortex in area 17 only. Neurons of this area project back ipsilaterally to the LGN and the superior colliculus (SC). No significant decrease in the activity of the cholinergic marker enzyme choline acetyltransferase could be observed under any of the experimental conditions; there was rather a tendency to increased activity in the subcortical centres. AChE as a less specific marker also exhibited no gross changes in activity in the lesioned animals. The results add more direct proof to pharmacological and physiological evidence that ACh is not involved in the synaptic transmission of the direct optic projections in rats, either at the subcortical or at the cortical level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00237699
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  • 6
    Electronic Resource
    Electronic Resource
    Cellular Distribution of 6-Phosphofructo-1-Kinase Isoenzymes in Rat Brain (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In the brain, all three isoenzyme types [muscle (M), liver (L), and brain (C)] of 6-phosphofructo-1-kinase (PFK; EC 2.7.1.11) occur, forming a complex mixture of homo- and heterotetramers. The PFK isoenzyme pattern of the different brain cell types is yet unknown. In the present study, we investigated the distribution of the PFK isoenzyme subunits in primary and secondary cell cultures and in bulk-isolated cells of rat brain by means of sodium dodecyl sulfate-polyacrylamide gel electrophoresis and western blotting. All three PFK isoenzymes are present in all cell types but in different proportions. The cellular distribution of the PFK isoenzymes in situ was studied immunohistochemically with different polyclonal antisera against purified rat PFKs. The monospecific antibody against M-type PFK stained preferentially the perinuclear areas of neurons and glial cells. The antibodies that in immunoblots detected mainly the L-type PFK showed a characteristic staining in only the cytoplasma and the processes of cells, whereas the C-type antibodies almost homogeneously stained whole cell bodies as well as large dendrites. Because the PFK isoenzymes differ with respect to their allosteric properties, their differential distribution in different brain cells might be of importance for the regulation of brain glycolysis in the different cellular compartments of the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.67062573.x
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  • 7
    Electronic Resource
    Electronic Resource
    THE INFLUENCE OF FUNCTIONAL ALTERATION ON MONOAMINE OXIDASE AND CATECHOL-O-METHYL TRANSFERASE IN THE VISUAL PATHWAY OF RATS (1974)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 22 (1974), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —Rats were reared in complete darkness or under chronic stimulation with flashing light from birth to the age of 7 weeks. Light deprivation caused a significant increase in monoamine oxidase activity (measured with [14C]serotonin) of about 30 per cent in the structures of the visual pathway. Chronic stimulation with flashing light had no influence on the activity of monoamine oxidase in either visual or non-visual structures. The activity of catechol-O-methyl transferase in the brain areas of light-deprived rats was reduced, in light-stimulated rats it was slightly increased. In mother rats kept together with their litters in either complete darkness or flashing light for 5 weeks no change in monoamine oxidase activity was observed. The activity of catechol-O-methyl transferase in mother rats kept in darkness was significantly decreased in all brain regions studied; in light-stimulated animals the enzyme activity was not affected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1974.tb06885.x
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  • 8
    Electronic Resource
    Electronic Resource
    SOME PROPERTIES OF SOLUBLE AND SOLUBILIZED PARTICLE-BOUND HEXOKINASE (1971)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Particle-bound hexokinase of rat brain homogenates was solubilized by successive treatment with 0-9 M-NaCl or 003 M-ATP (pH 8.0) and 0-5% (w/v) Triton X-100. This solubilized hexokinase and the soluble hexokinase present in cytoplasm of rat brain homogenates were chromatographed on DEAE-cellulose and some kinetic properties of the isolated hexokinase peaks were studied. The chromatographic separation was greatly influenced by the EDTA-concentration of the buffer used. No significant differences were observed in the chromatographic pattern and in the apparent Km-values for ATP and glucose and the apparent Kt for glucose-6-phosphate (versus ATP) between the soluble and particulate hexokinase solubilized by different reagents. On agarose-electrophoresis the solubilized particulate enzyme migrates as one single band, the soluble hexokinase separates into one major and two minor bands.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1971.tb12002.x
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  • 9
    Electronic Resource
    Electronic Resource
    Protein kinase Cα and β1 isoforms are regulators of α-secretory proteolytic processing of amyloid precursor protein in vivo (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have recently shown that in utero treatment of guinea pigs with the DNA methylating substance methylazoxymethanol acetate (MAM) results in neocortical microencephalopathy, increased protein kinase C (PKC) activity and altered processing of the amyloid precursor protein (APP) in neocortex of offspring. Here we show that PKCα and PKCβ1 are the key regulators of α-secretory APP processing in guinea pig neocortex under these experimental conditions in vivo. This conclusion is based on the selective translocation of PKCα and PKCβ1 isoforms to the cell membrane in MAM-treated guinea pigs, as revealed by Western blot analysis and by immunocytochemistry. Additionally, we observed that [3H]phorbol ester binding to protein kinase C increased by 38% and enhanced basal PKC activity by 58% in the neocortex of microencephalic guinea pigs. Inhibition of PKCα/PKCβ1 by Gö6976 abolished this difference, suggesting that constitutive overactivation of these PKC isoforms accounts for the increase in total PKC activity. We also observed a strong positive correlation between levels of α-secretase-processed APP and PKC activity in the neocortex of individual animals, providing further evidence for a significant role of classical PKC isoforms in nonamyloidogenic APP processing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0953-816x.2001.01525.x
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  • 10
    Electronic Resource
    Electronic Resource
    Increased neuronal and glial expression of protein kinase C isoforms in neocortex of transgenic Tg2576 mice with amyloid pathology (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We investigated the influence of five- to sevenfold neuronal overexpression of the Swedish mutation of human APP695 (APPsw) in the transgenic mouse strain Tg2576 on neocortical protein kinase C (PKC) expression and subcellular distribution. Using specific antibodies to PKCα, PKCβ, PKCγ, PKCε and PKCζ isoforms for Western blot analysis, we observed increased immunoreactivity for PKCα and PKCγ isoforms in crude tissue homogenates from the neocortex of 16-month-old APPsw mice as compared with nontransgenic littermates, which was not present in 6 month-old Tg2576 mice. We also observed elevated levels of PKCα, PKCβ, PKCγ and PKCζ in membrane fractions and reduced concentrations of PKCα and PKCγ in cytosolic fractions of aged Tg2576 mice, indicating that these PKC isoforms are in their activated state. In young, 6-month-old Tg2576 mice, however, the increase in membrane-bound PKC isoforms and concomitant decrease in cytosolic PKC isoforms was much less pronounced, demonstrating the age-dependent nature of alterations in PKC isoforms. Immunocytochemistry of brain sections supported these findings and revealed increased neuronal labelling for PKCα, PKCγ and PKCλ isoforms in neocortex of 16-month-old APPsw mice compared with nontransgenic littermates, with the increase being strongest for PKCγ and PKCλ isoforms. Additionally, PKCγ and to a lesser extent PKCλ isoforms were induced in reactive astrocytes in proximity to amyloid plaques. Our data indicate that neuronal overexpression of APPsw causes a dynamic change in neuronal expression and activation of multiple PKC isoforms known to be regulators of proteolytic amyloid precursor protein (APP) processing (PKCα) and of neuronal survival (PKCλ and PKCζ). The induction of the PKCγ and PKCλ isoforms in reactive astrocytes surrounding amyloid plaques might be required for astrocyte activation and astrocytic cytokine expression in response to amyloid plaque formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2001.01388.x
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