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Cell and Animal Models in Aging and Dementia Research

  • Conference proceedings
  • © 1994

Overview

Editors:
  1. S. Hoyer

    1. Institute for Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Federal Republic of Germany

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  2. D. Müller

    1. Institute for Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Federal Republic of Germany

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  3. K. Plaschke

    1. Institute for Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Federal Republic of Germany

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Part of the book series: Journal of Neural Transmission. Supplementa (NEURAL SUPPL, volume 44)

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Table of contents (20 papers)

  1. Front Matter

    Pages I-VIII
    Download chapter PDF

  2. Primary cultures of neurons for testing neuroprotective drug effects

    • H. Oberpichler-Schwenk, J. Krieglstein
    Pages 1-20

  3. Regulation of proteolytic processing of the amyloid β-protein precursor of Alzheimer’s disease in transfected cell lines and in brain slices

    • R. M. Nitsch, B. E. Slack, S. A. Farber, J. G. Schulz, M. Deng, C. Kim et al.
    Pages 21-27

  4. Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration

    • V. L. Smith-Swintosky, M. P. Mattson
    Pages 29-45

  5. An aggregate brain cell culture model for studying neuronal degeneration and regeneration

    • S. S. Chatterjee, M. Nöldner
    Pages 47-60

  6. The organotypic entorhinal-hippocampal complex slice culture of adolescent rats. A model to study transcellular changes in a circuit particularly vulnerable in neurodegenerative disorders

    • S. Diekmann, R. Nitsch, T. G. Ohm
    Pages 61-71

  7. The use of ion-sensitive electrodes and fluorescence imaging in hippocampal slices for studying pathological changes of intracellular Ca2+ regulation

    • P. Schubert, F. Keller, Y. Nakamura, K. Rudolphi
    Pages 73-85

  8. The cultured fibroblast model

    • J. P. Blass
    Pages 87-95

  9. Psychometric testing in rats during normal ageing Procedures and results

    • H. Bubna-Littitz, J. Jahn
    Pages 97-109

  10. Ultrastructural changes in brain parenchyma during normal aging and in animal models of aging

    • C. Struys-Ponsar, A. Florence, A. Gauthier, R. R. Crichton, Ph. van den Bosch de Aguilar
    Pages 111-132

  11. Morphological hippocampal changes during normal aging and their relation to cognitive deterioration

    • T. Kadar, I. Arbel, M. Silbermann, A. Levy
    Pages 133-143

  12. The function of the NMDA-receptor during normal brain aging

    • W. E. Müller, S. Stoll, K. Scheuer, A. Meichelböck
    Pages 145-158

  13. Age-related alterations by chronic intermittent hypoxia on cerebral synaptosomal ATPase activities

    • G. Benzi, A. Gorini, R. Arnaboldi, B. Ghigini, R. F. Villa
    Pages 159-171

  14. Impairment in memory function and neurodegenerative changes in the cholinergic basal forebrain system induced by chronic intake of ethanol

    • T. Arendt
    Pages 173-187

  15. Dysfunction of the brain cholinergic system during aging and after lesions of the nucleus basalis of Meynert

    • G. Pepeu, I. Marconcini Pepeu
    Pages 189-194

  16. Receptor function in cortical rat brain regions after lesion of nucleus basalis

    • R. Schliebs, T. Feist, S. Roßner, V. Bigl
    Pages 195-208

  17. Trophic factors during normal brain aging and after functional damage

    • R. Hellweg
    Pages 209-217

  18. Alzheimer’s disease and transgenic mice

    • Ch. Czech, C. Masters, K. Beyreuther
    Pages 219-230

  19. An aspect of Alzheimer neuropathology after suicide transport damage

    • I. P. Chessell, P. T. Francis, M-T. Webster, A. W. Procter, P. R. Heath, R. C. A. Pearson et al.
    Pages 231-243

  20. AF64A-induced brain damage and its relation to dementia

    • H. Hörtnagl
    Pages 245-257
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Keywords

About this book

Although age has been recognized as a risk factor for late-onset dementia of Alzheimer type, its etiology is unknown as yet. Several age-related metabolic abnormalities may thus become important for the pathogenesis of the late-onset form. Studies at the cellular/molecular level in brain tissue are possible post mortem, but lack information on the beginning of the disorder. In this supplement, different approaches are dealt with how to induce structural and/or metabolic abnormalities in relevant cell cultures, in brain slices and in experimental animals, and how behavioral changes parallel the metabolic variations.

Editors and Affiliations

  • Institute for Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Federal Republic of Germany

    S. Hoyer, D. Müller, K. Plaschke

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