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Advances in Down Syndrome Research

  • Book
  • © 2003

Overview

Editors:
  1. G. Lubec

    1. Department of Pediatrics, University of Vienna, Vienna, Austria

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Part of the book series: Journal of Neural Transmission. Supplementa (NEURAL SUPPL, volume 67)

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Table of contents (21 chapters)

  1. Front Matter

    Pages I-X
    Download chapter PDF

  2. A new mouse model for Down syndrome

    • Y. Kazuki, T. C. Schulz, T. Shinohara, M. Kadota, R. Nishigaki, T. Inoue et al.
    Pages 1-20

  3. Predicting pathway perturbations in Down syndrome

    • K. Gardiner
    Pages 21-37

  4. Aberrant protein expression of transcription factors BACH1 and ERG, both encoded on chromosome 21, in brains of patients with Down syndrome and Alzheimer’s disease

    • K. S. Shim, R. Ferrando-Miguel, G. Lubec
    Pages 39-49

  5. Cell cycle and cell size regulation in Down Syndrome cells

    • M. Rosner, A. Kowalska, A. Freilinger, A-R. Prusa, E. Marton, M. Hengstschläger
    Pages 51-58

  6. Transcription factor REST dependent proteins are comparable between Down Syndrome and control brains: challenging a hypothesis

    • S. Y. Sohn, R. Weitzdoerfer, N. Mori, G. Lubec
    Pages 59-66

  7. An altered antioxidant balance occurs in Down syndrome fetal organs: Implications for the “gene dosage effect” hypothesis

    • J. B. de Haan, B. Susil, M. Pritchard, I. Kola
    Pages 67-83

  8. Overexpression of C1-tetrahydrofolate synthase in fetal Down Syndrome brain

    • M. Fountoulakis, T. Gulesserian, G. Lubec
    Pages 85-93

  9. Increased expression of human reduced folate carrier in fetal Down syndrome brain

    • G. Lubec, M. Bajo, M. S. Cheon, H. Bajova, L. H. Matherly
    Pages 95-103

  10. Chromosome 21 KIR channels in brain development

    • E. Thiery, S. Thomas, S. Vacher, A.-L. Delezoide, J. M. Delabar, N. Créau
    Pages 105-115

  11. Reduction of chromatin assembly factor 1 p60 and C21orf2 protein, encoded on chromosome 21, in Down Syndrome brain

    • K. S. Shim, J. M. Bergelson, M. Furuse, V. Ovod, T. Krude, G. Lubec
    Pages 117-128

  12. The MNB/DYRK1A protein kinase: Neurobiological functions and Down syndrome implications

    • B. Hämmerle, C. Elizalde, J. Galceran, W. Becker, F. J. Tejedor
    Pages 129-137

  13. The MNB/DYRK1A protein kinase: Genetic and biochemical properties

    • J. Galceran, K. de Graaf, F. J. Tejedor, W. Becker
    Pages 139-148

  14. Cytoskeleton derangement in brain of patients with Down Syndrome, Alzheimer’s disease and Pick’s disease

    • D. Pollak, N. Cairns, G. Lubec
    Pages 149-158

  15. The cerebral cortex in Fetal Down Syndrome

    • U. Unterberger, G. Lubec, M. Dierssen, G. Stoltenburg-Didinger, J. C. Farreras, H. Budka
    Pages 159-163

  16. Polysomnography in transgenic hSOD1 mice as Down syndrome model

    • D. Colas, J. London, R. Cespuglio, N. Sarda
    Pages 165-171

  17. Spectrum of cognitive, behavioural and emotional problems in children and young adults with Down syndrome

    • R. Nicham, R. Weitzdörfer, E. Hauser, M. Freidl, M. Schubert, E. Wurst et al.
    Pages 173-191

  18. Overexpression of transcription factor BACH1 in fetal Down Syndrome brain

    • R. Ferrando-Miguel, M. S. Cheon, J.-W. Yang, G. Lubec
    Pages 193-205

  19. Down syndrome and associated congenital malformations

    • B. L. Shapiro
    Pages 207-214

  20. RNA Microarray analysis of channels and transporters in normal and fetal Down Syndrome (trisomy 21) brain

    • G. Lubec, S. Y. Sohn
    Pages 215-224
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Keywords

About this book

"Advances in Down Syndrome Research” represents updated research in several areas of Down Syndrome (DS). A new promising animal model of DS is reported and this opens new opportunities to study pathomechanisms and pharmacological approaches as it is more than difficult to carry out studies in humans and the clinical features are highly variable. In terms of biology, cell cycle and stem cell studies and in terms of biochemistry, relevance of studies on a specific protein kinase, channels, transporters, superoxide dismutase, antioxidant system, chromosome assembly factor and other important biological structures are provided. And again, the gene dosage hypothesis is addressed and although the vast majority of chromosome 21 gene products is unchanged in fetal DS brain, a few specific chromosome 21 encoded structures including transcription factors are indeed overexpressed although findings in fetal DS are different from those in adult DS brain when Alzheimer-like neuropathology supervenes.

Editors and Affiliations

  • Department of Pediatrics, University of Vienna, Vienna, Austria

    G. Lubec

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