Protein Expression in Down Syndrome Brain

  • Gert Lubec

Table of contents

  1. Front Matter
    Pages I-X
  2. M. Freidl, T. Gulesserian, G. Lubec, M. Fountoulakis, B. Lubec
    Pages 47-57
  3. P. G. Nelson, S. K. McCune, A. M. Ades, K. B. Nelson
    Pages 85-94
  4. S. H. Kim, M. Fountoulakis, M. Dierssen, G. Lubec
    Pages 109-116
  5. M. Dierssen, E. Martí, C. Pucharcós, V. Fotaki, X. Altafaj, K. Casas et al.
    Pages 131-148
  6. E. Engidawork, N. Balic, J.-F. Juranville, M. Fountoulakis, M. Dierssen, G. Lubec
    Pages 149-162
  7. T. Gulesserian, E. Engidawork, B. C. Yoo, N. Cairns, G. Lubec
    Pages 163-179
  8. E. Kitzmueller, S. Greber, G. Lubec, M. Fountoulakis
    Pages 203-210
  9. G. Bernert, M. Sustrova, E. Sovcikova, R. Seidl, G. Lubec
    Pages 237-245
  10. R. Seidl, N. Cairns, G. Lubec
    Pages 247-261
  11. S. H. Kim, A. C. Nairn, N. Cairns, G. Lubec
    Pages 263-272
  12. S. H. Kim, M. Dierssen, J. C. Ferreres, M. Fountoulakis, G. Lubec
    Pages 273-280
  13. M. S. Cheon, M. Fountoulakis, N. J. Cairns, M. Dierssen, K. Herkner, G. Lubec
    Pages 281-288
  14. M. S. Cheon, M. Fountoulakis, M. Dierssen, J. C. Ferreres, G. Lubec
    Pages 311-319
  15. Back Matter
    Pages 373-374

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.


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

  • Gert Lubec
    • 1
  1. 1.Universität-KinderklinikWienAustria

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