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  • 1
    Electronic Resource
    Electronic Resource
    Induction of epitopes associated with neurofibrillary tangles in clonal mouse neuroblastoma (S20Y) cells (1990)
    Springer
    Acta neuropathologica 81 (1990), S. 30-40 
    Details
    ISSN: 1432-0533
    Keywords: Neuroblastoma cultures ; Neurofibrillary tangles ; Paired helical filaments ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Accumulation of paired helical filaments (PHF) in neurofibrillary tangles is a key neuropathological hallmark in Alzheimer's disease (AD). To date, PHF have been found primarily in humans. Cultured murine cholinergic neuroblastoma (S20Y) cells, following exposure to a serum-free medium or a differentiation medium, developed immunoreactivity to anti-PHF antibodies, and to the Alz-50 by immunocytochemical and immunoblot analyses. Electron microscopic examination revealed abundant fascicles of 10-nm filaments coursing tortuously amongst organelles, such as mitochondria, endoplasmic reticulum and dense-core vesicles, in perikarya and in neuritic extensions. However, subcellular structures identical or similar to PHF could not be found in these non-human cells. This convenient cell culture model may prove to be useful for studying certain aspects of the mechanisms underlying the abnormal cytoskeletal alterations which are characteristic of AD and related neurodegenerative disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00662635
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  • 2
    Electronic Resource
    Electronic Resource
    Iatrogenic Nutritional Deficiencies (1982)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Nutrition 2 (1982), S. 201-227 
    Details
    ISSN: 0199-9885
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.nu.02.070182.001221
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  • 3
    Electronic Resource
    Electronic Resource
    FATTY ACID COMPOSITION OF CEREBROSIDES IN MICROSOMES AND MYELIN OF MOUSE BRAIN (1970)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 17 (1970), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The fatty acid composition of cerebrosides isolated from myelin and from light and heavy microsomes of adult mouse brain was determined. 2-Hydroxy fatty acids represented 80 per cent of the fatty acids in myelin cerebrosides and approximately 55 per cent of the fatty acids in both light and heavy microsomes. In myelin, the majority of the fatty acids, both normal and hydroxy, were of chain length 〉 C-20; in microsomes, shorter chain acids (C-16 to C-20) predominated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1970.tb00533.x
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  • 4
    Electronic Resource
    Electronic Resource
    INHIBITION OF ACETYLCHOLINE SYNTHESIS AND OF CARBOHYDRATE UTILIZATION BY MAPLE-SYRUP-URINE DISEASE METABOLITES (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 26 (1976), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The branched-chain 2-oxo acids which accumulate in maple-syrup-urine disease inhibited the production of acetylcholine and of lipids, proteins, nucleic acids and of CO2. in sliced adult rat brains incubated with [U-14C] glucose. Inhibition of the biosynthetic reactions was proportional to the inhibition of CO2 production, even though the flux of radioactivity into the biosynthetic products was less than 2% of that to CO2.The oxo acids reduced the production of 14CO2, from [U-14C] glucose and from [2-14C]pyruvic acid more than from [1-14C]pyruvic acid in sliced brains. They inhibited the solubilized oxoglutarate dehydrogenase complex more than they did the solubilized pyruvate dehydrogenase complex. Valine and isoleucine, which also accumulate in maple-syrup-urine disease, inhibited pyruvate kinase from rat brain allosterically. Quantitative comparison of the effects of the disease metabolites on cell-free systems with their effects on fluxes in intact cells indicated that the inhibition of oxoglutarate dehydrogenase appeared to be functionally significant. The residual activities of the other enzymes studied were adequate to support the normal flux of carbohydrates.The oxo acids were effective at concentrations within the range reported to occur in patients with maple-syrup-urine disease. The effects on biosyntheses including that of acetylcholine would be expected to impair brain development and function and could be important in the development of brain disease in the patients. In contrast to the results with metabolites from maple-syrup-urine disease, metabolites which accumulate in phenylketonuria (phenylalanine and 2-oxo-3-phenylpropionic acid) did not inhibit carbohydrate utilization or the biosynthetic reactions studied, under the conditions of these experiments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1976.tb06988.x
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  • 5
    Electronic Resource
    Electronic Resource
    IMPAIRED SYNTHESIS OF ACETYLCHOLINE IN BRAIN ACCOMPANYING MILD HYPOXIA AND HYPOGLYCEMIA (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 27 (1976), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Lowering the concentration of oxygen or of glucose to which mouse and rat brains were exposed impaired the synthesis of acetylcholine from labelled precursors in vivo.Histotoxic hypoxia induced with KCN or anemic hypoxia induced with NaNO2 (to oxidize hemoglobin to methemoglobin) reduced incorporation of [2H4]choline into acetylcholine. This change in acetylcholine metabolism occurred with doses of KCN or NaNO2 which did not alter the concentrations of ATP or ADP or the adenylate energy charge. Hypoglycemia induced by large doses of insulin also reduced the incorporation of [2H4]choline into acetylcholine. Both hypoxia and hypoglycemia increased the concentration of choline in the brain. The specific activity of choline did not decrease in hypoxia; it did not decrease enough in hypoglycemia to explain the reduced incorporation of [2H4]choline into acetylcholine.Pretreatment with the cholinesterase inhibitor physostigmine delayed the onset of both seizures and death in mice after induction of hypoxia by large doses of NaNO2. Pretreatment with physostigmine also decreased the number of mice dying within 3 h after the induction of hypoglycemia with large doses of insulin. These observations suggest that the effects of hypoxia and hypoglycemia interfere with the synthesis of a critical pool of acetylcholine.The incorporation of labelled precursors into acetylcholine related linearly to both the cytoplasmic redox state (NAD/NADH ratio) and to the NAD/NADH potential across the mitochondrial membrane. The redox potential of NAD/NADH in the cytoplasm was calculated from the [pyruvate]/[lactate] equilibrium and the redox potential of NAD/NADH in the mitochondria from the [NH4][2-oxoglutar-ate]/[glutamate] equilibrium. The potential across the mitochondrial membrane was calculated from the difference.These observations indicate that carbohydrate oxidation is one of the factors on which the synthesis of the neurotransmitter acetylcholine depends closely in mouse and rat brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1976.tb01540.x
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  • 6
    Electronic Resource
    Electronic Resource
    THE REGULATION OF PYRUVATE DEHYDROGENASE IN BRAIN IN VIVO (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 26 (1976), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The activity of pyruvate dehydrogenase in the brains of mice frozen in liquid nitrogen was 14·0 nmol/min per mg protein. It rose to 23·8 nmol/min per mg protein after incubation of the brain homogenate with 10mm-MgCl2 to activate (dephosphorylate) the enzyme, indicating that approx 60% of the enzyme was originally in the active form. Treatment with amobarbital or pentobarbital halved the proportion of pyruvate dehydrogenase in the active form. The proportion of pyruvate dehydrogenase in the active form increased during ischemia, activation being complete within one min. Anesthesia with amobarbital slowed the activation during ischemia but did not alter the total amount of pyruvate dehydrogenase activity. The concentration of ATP, the ATP/ADP ratio and the adenylate energy charge increased as the proportion of pyruvate dehydrogenase in the active form decreased during barbiturate anesthesia, and they decreased as the proportion of pyruvate dehydrogenase in the active form increased during ischemia. After treatment with insulin, the proportion of pyruvate dehydrogenase in the active form increased by 30%. but the energy charge did not change. Treatment of mice with ether, morphine, ethanol, or diazepam did not change the proportion of pyruvate dehydrogenase in the active form although these treatments have been reported to alter pyruvate oxidation in brain in vivo. Treatments which altered pyruvate oxidation in the brain did not consistently alter the proportion of pyruvate dehydrogenase in the active form, unless they also altered energy charge.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1976.tb04440.x-i1
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  • 7
    Electronic Resource
    Electronic Resource
    Abnormalities of mitochondrial enzymes in Alzheimer disease (1998)
    Springer
    Journal of neural transmission 105 (1998), S. 855-870 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Alzheimer's disease ; mitochondria ; α-ketoglutarate dehydrogenase ; cytochrome oxidase ; pyruvate dehydrogenase ; neurodegenerative disease.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Abundant evidence, including critical information gathered by Prof. Siegfried Hoyer and his colleagues, indicates that abnormalities of cerebral metabolism are common in neurodegenerative diseases, including Alzheimer's Disease (AD). Alterations in mitochondrial enzymes likely underlie these deficits. Replicable reductions in AD brain occur in the pyruvate dehydrogenase complex (the link of glycolysis to the Kreb's cycle), the α-ketoglutarate dehydrogenase complex (KGDHC; the link of Kreb's cycle to glutamate metabolism) and cytochrome oxidase (the link of the Kreb's cycle to oxygen utilization). Available evidence suggests that deficiencies in KGDHC may be genetic in some cases, whereas evidence that the other two enzyme systems have a genetic component is lacking. Additional results indicate that the reductions can also be secondary to other causes including oxidative stress. A variety of data suggest that the mitochondrial insufficiencies contribute significantly to the pathophysiology of AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050099
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  • 8
    Electronic Resource
    Electronic Resource
    A reproducible procedure for primary culture and subsequent maintenance of multiple lines of human skin fibroblasts (1998)
    Springer
    Age 21 (1998), S. 7-14 
    Details
    ISSN: 1574-4647
    Keywords: Fibroblasts ; Alzheimer’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cultured fibroblasts are a valuable tool to study many cellular processes and their modification by aging. Fibroblasts are a useful cell type in which to study many diseases, including those of the nervous system, in which a strong genetic component is suspected. Fibroblasts permit the study of multiple, dynamic processes in living cells, while avoiding the effect of the dying process and post-mortem artifacts that limit other approaches. For results to be comparable across time in one laboratory or consistent between laboratories, the detailed culture techniques require meticulous care and replicability. Lack of attention to detail in initial stages can lead to selection of different cell populations. Small variations in othe variables such as batches of serum can significantly alter growth rates and comparisons of cells from controls and Alzheimer patients. The aim of this paper is to present a detailed protocol for comparison of multiple cell lines from many patients. An example of using this approach to study growth and phase out (i.e., senescence) of cells from Alzheimer patients is presented. This procedure represents a modification of an earlier protocol (Cristofalo and Charpentier, 1980).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s11357-998-0002-z
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