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  • © 2001

Protein Expression in Down Syndrome Brain

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  • ISBN: 978-3-7091-6262-0
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Table of contents (30 chapters)

  1. Front Matter

    Pages I-X
  2. 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
  3. Glial-neurotrophic mechanisms in Down syndrome

    • P. G. Nelson, S. K. McCune, A. M. Ades, K. B. Nelson
    Pages 85-94
  4. 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
  5. 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
  6. 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
  7. 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
  8. Carbohydrate handling enzymes in fetal Down Syndrome brain

    • E. Kitzmueller, S. Greber, G. Lubec, M. Fountoulakis
    Pages 203-210
  9. 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

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.

Keywords

  • Alzheimer Krankheit
  • Alzheimer's disease
  • Chromosom 21
  • Down Syndrom
  • Down syndrome
  • chromosome 21
  • fetal Down syndrome/Protein Expression
  • protein expression
  • Alzheimer´s disease
  • brain
  • chromosome
  • development
  • Elongation
  • neuropathology
  • protein
  • RNA
  • Syndrom
  • syndromes
  • Termination
  • tissue
  • transcription

Editors and Affiliations

  • Universität-Kinderklinik, Wien, Austria

    Gert Lubec

Bibliographic Information

Buying options

eBook USD 199.00
Price excludes VAT (USA)
  • ISBN: 978-3-7091-6262-0
  • Instant PDF download
  • Readable on all devices
  • Own it forever
  • Exclusive offer for individuals only
  • Tax calculation will be finalised during checkout
Hardcover Book USD 259.00
Price excludes VAT (USA)