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Protein Expression in Down Syndrome Brain

  • Book
  • © 2001

Overview

Editors:
  1. Gert Lubec

    1. Universität-Kinderklinik, Wien, Austria

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Table of contents (30 chapters)

  1. Front Matter

    Pages I-X
    Download chapter PDF

  2. Decreased alpha-endosulfine, an endogenous regulator of ATP-sensitive potassium channels, in brains from adult Down syndrome patients

    • S. H. Kim, G. Lubec
    Pages 1-9

  3. Developmental instability of the cerebellum and its relevance to Down syndrome

    • B. L. Shapiro
    Pages 11-34

  4. Expression of the multidrug resistance P glycoprotein (Pgp) and multidrug resistance associated protein (MRP1) in Down syndrome brains

    • E. Engidawork, J. C. Roberts, R. Hardmeier, R. J. Scheper, G. Lubec
    Pages 35-45

  5. Deterioration of the transcriptional, splicing and elongation machinery in brain of fetal Down Syndrome

    • M. Freidl, T. Gulesserian, G. Lubec, M. Fountoulakis, B. Lubec
    Pages 47-57

  6. Fetal life in Down Syndrome starts with normal neuronal density but impaired dendritic spines and synaptosomal structure

    • R. Weitzdoerfer, M. Dierssen, M. Fountoulakis, G. Lubec
    Pages 59-70

  7. Antioxidant proteins in fetal brain: superoxide dismutase-1 (SOD-1) protein is not overexpressed in fetal Down syndrome

    • T. Gulesserian, E. Engidawork, M. Fountoulakis, G. Lubec
    Pages 71-84

  8. Glial-neurotrophic mechanisms in Down syndrome

    • P. G. Nelson, S. K. McCune, A. M. Ades, K. B. Nelson
    Pages 85-94

  9. Aberrant expression of dihydropyrimidinase related proteins-2,-3 and -4 in fetal Down Syndrome brain

    • R. Weitzdoerfer, M. Fountoulakis, G. Lubec
    Pages 95-107

  10. Decreased protein levels of complex I 30-kDa subunit in fetal Down syndrome brains

    • S. H. Kim, M. Fountoulakis, M. Dierssen, G. Lubec
    Pages 109-116

  11. Selective upregulation of the ubiquitin-proteasome proteolytic pathway proteins, proteasome zeta chain and isopeptidase T in fetal Down syndrome

    • E. Engidawork, J.-F. Juranville, M. Fountoulakis, M. Dierssen, G. Lubec
    Pages 117-130

  12. Functional genomics of Down syndrome: a multidisciplinary approach

    • M. Dierssen, E. Martí, C. Pucharcós, V. Fotaki, X. Altafaj, K. Casas et al.
    Pages 131-148

  13. Unaltered expression of Fas (CD95/APO-1), Caspase-3, Bcl-2 and Annexins in brains of fetal Down syndrome: evidence against increased apoptosis

    • E. Engidawork, N. Balic, J.-F. Juranville, M. Fountoulakis, M. Dierssen, G. Lubec
    Pages 149-162

  14. Alteration of caspases and other apoptosis regulatory proteins in Down syndrome

    • T. Gulesserian, E. Engidawork, B. C. Yoo, N. Cairns, G. Lubec
    Pages 163-179

  15. Expression of apoptosis related proteins: RAIDD, ZIP kinase, Bim/BOD, p21, Bax, Bcl-2 and NF-kB in brains of patients with Down syndrome

    • E. Engidawork, T. Gulesserian, R. Seidl, N. Cairns, G. Lubec
    Pages 181-192

  16. Increased brain protein levels of carbonyl reductase and alcohol dehydrogenase in Down Syndrome and Alzheimer’s disease

    • B. Balcz, L. Kirchner, N. Cairns, M. Fountoulakis, G. Lubec
    Pages 193-201

  17. Carbohydrate handling enzymes in fetal Down Syndrome brain

    • E. Kitzmueller, S. Greber, G. Lubec, M. Fountoulakis
    Pages 203-210

  18. Changes in nicotinic acetylcholine receptor subunits expression in brain of patients with Down syndrome and Alzheimer’s disease

    • E. Engidawork, T. Gulesserian, N. Balic, N. Cairns, G. Lubec
    Pages 211-222

  19. Protein levels of human peroxiredoxin subtypes in brains of patients with Alzheimer’s disease and Down Syndrome

    • S. H. Kim, M. Fountoulakis, N. Cairns, G. Lubec
    Pages 223-235

  20. Effects of a single transdermal nicotine dose on cognitive performance in adults with Down syndrome

    • G. Bernert, M. Sustrova, E. Sovcikova, R. Seidl, G. Lubec
    Pages 237-245
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Keywords

About this book

When we worked on Down Syndrome brain in the past we have been focus­ ing on adult brain. This was a major step forwards as most work on Down Syndrome was carried out on fibroblasts or other tissues and, moreover, we introduced proteomics to identify and quantify brain protein expression. We considered evaluation of brain protein expression in Down Syndrome brain by and by more important than gene hunting at the nucleic acid level realiz­ ing the long unpredictable way from RNA to protein. The availability of fetal samples along with the proteomic appproach stimulated and reinforced studies on Down Syndrome brain. And indeed, it was found out that some observations on aberrant protein expression in adult Down Syndrome brain could not be verified in the fetal samples indi­ cating that neurodegeneration in adult Down Syndrome brain may have been responsible rather than trisomy 21. Using brains from the early second trimester of gestation led to the generation of a series of clues for the under­ standing of aberrant wiring of the brain in Down Syndrome and enabled the determination of altered key functions in early life; e. g. undetectably low drebrin was observed in Down Syndrome cortex, an integral constituent and marker for dendritic spines, main effectors of cross-talk between neurons. In addition, evaluation of the nature of the neuronal deficits in terms of neuro­ transmission markers could be established as well as neuronal density in fetal Down Syndrome cortex.

Editors and Affiliations

  • Universität-Kinderklinik, Wien, Austria

    Gert Lubec

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