Beta-amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Tursonjan Tokay, Olfa Masmoudi, Pierrick Gandolfo, Jérôme Leprince, Georges Pelletier, Hubert Vaudry, Marie Christine Tonon

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


Accumulation of β-amyloid peptide (Aβ), which is a landmark of Alzheimer's disease, may alter astrocyte functions before any visible symptoms of the disease occur. Here, we examined the effects of Aβ on biosynthesis and release of diazepam-binding inhibitor (DBI), a polypeptide primarily expressed by astroglial cells in the CNS. Quantitative RT-PCR and specific radioimmunoassay demonstrated that aggregated Aβ25-35, at concentrations up to 10-4 M, induced a dose-dependent increase in DBI mRNA expression and DBI-related peptide release from cultured rat astrocytes. These effects were totally suppressed when aggregation of Aβ 25-35 was prevented by Congo red. Measurement of the number of living cells revealed that Aβ25-35 induced a trophic rather than a toxic effect on astrocytes. Administration of cycloheximide blocked Aβ25-35-induced increase of DBI gene expression and endozepine accumulation in astrocytes, indicating that protein synthesis is required for DBI gene expression. Altogether, the present data suggest that Aβ-induced activation of endozepine biosynthesis and release may contribute to astrocyte proliferation associated with Alzheimer's disease.

Original languageEnglish
Pages (from-to)607-616
Number of pages10
JournalJournal of Neurochemistry
Issue number3
Publication statusPublished - Aug 2005


  • Astrocytes
  • Diazepam-binding inhibitor
  • Octadecaneuropeptide
  • β-amyloid protein

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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