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Related Experiment Videos

BACE-2 is overexpressed in Down's syndrome.

L Barbiero1, L Benussi, R Ghidoni

  • 1Neurobiology Laboratory, Memory Clinic, IRCCS Centro S. Giovanni di Dio-FbF, Brescia, Italy.

Experimental Neurology
|August 5, 2003
PubMed
Summary

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Down's syndrome (DS) patients show increased BACE-2 mRNA and extracellular protein levels. This BACE-2 overexpression in DS may contribute to amyloid-beta plaque formation in the brain.

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Amyloid-beta (Abeta) protein deposition is common in Down's syndrome (DS).
  • Beta-site amyloid precursor protein cleaving enzyme 2 (BACE-2) is involved in Abeta processing and its gene is located on chromosome 21.
  • BACE-2 cleaves amyloid precursor protein at the beta site and other sites.

Purpose of the Study:

  • To characterize BACE-2 gene and protein expression in Down's syndrome patients.
  • To investigate the role of BACE-2 in the extracellular compartment in DS.

Main Methods:

  • Nonradioactive ribonuclease protection assay to quantify BACE-2 mRNA in fibroblasts.
  • Western blot analysis to assess intracellular and extracellular BACE-2 protein levels.
  • Analysis of BACE-2 expression in DS fetal brains and neural stem cells.

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Main Results:

  • BACE-2 mRNA levels were 2.6-fold higher in DS fibroblasts compared to controls.
  • No significant difference in intracellular BACE-2 protein levels between DS and control groups.
  • Increased secretion of extracellular BACE-2 protein, with two distinct molecular weights, was observed in DS fibroblasts, fetal brains, and neural stem cells.

Conclusions:

  • BACE-2 mRNA is upregulated in Down's syndrome.
  • Extracellular BACE-2 overexpression in DS patients suggests a potential role in amyloid plaque formation.
  • The extracellular compartment is critical for understanding BACE-2's function in DS pathogenesis.