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Decreased protein levels of stathmin in adult brains with Down syndrome and Alzheimer’s disease

  • M. S. Cheon
  • M. Fountoulakis
  • N. J. Cairns
  • M. Dierssen
  • K. Herkner
  • G. Lubec
Chapter

Summary

Stathmin, distributed in neurons with high abundance, acts as an intracellular relay, integrating various transduction pathways triggered by extracellular signals and it is involved in physiological regulation of microtubule destabilization. Stathmin has been also shown to be a critical molecule in pathology of neurodegeneration such as Alzheimer’s disease (AD), particularly, in neurofibrillary tangle (NFT) formation. Here we evaluated protein levels of stathmin in adult brain from patients with AD and Down syndrome (DS) showing AD-like pathology by applying proteomic technologies with two-dimensional (2-D) gel electrophoresis, matrix-assisted laser desorption ionization mass spectroscopy (MALDI-MS) identification and specific software for quantification of proteins. Significantly decreased protein levels of stathmin were observed in frontal (2.12 ± 1.17, n = 6) and temporal (3.05 ± 2.81, n = 10) cortices of AD compared to controls (frontal cortex: 4.41 ± 1.70, n = 8; temporal cortex: 5.26 ± 2.26, n = 13). Stathmin was also significantly decreased in frontal (2.47 ± 1.11, n = 7) and temporal (2.02 ± 1.18, n = 9) cortices of DS. We also investigated stathmin levels in fetal brain. Stathmin was not significantly changed between fetal DS brain and controls. We suggest that the decreased protein level of stathmin in brains is associated with tangle formation and microtubule instability in DS as well as AD, but stathmin is not involved in the abnormal development of fetal DS brain.

Keywords

Down Syndrome Fetal Brain Neurobiol Aging Down Syndrome Patient Decrease Protein Level 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag/Wien 2001

Authors and Affiliations

  • M. S. Cheon
    • 1
  • M. Fountoulakis
    • 2
  • N. J. Cairns
    • 3
  • M. Dierssen
    • 4
  • K. Herkner
    • 1
  • G. Lubec
    • 1
  1. 1.Department of PediatricsUniversity of ViennaAustria
  2. 2.F. Hoffmann - La RocheBaselSwitzerland
  3. 3.Institute of Psychiatry, Brain BankKing’s CollegeUK
  4. 4.Medical and Molecular Genetics Center-IROHospital Duran i ReynalsBarcelonaSpain

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