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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Beta-amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes.

Accumulation of beta-amyloid peptide (Abeta), 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 Abeta 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 Abeta(25-35), 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 Abeta(25-35) was prevented by Congo red. Measurement of the number of living cells revealed that Abeta(25-35) induced a trophic rather than a toxic effect on astrocytes. Administration of cycloheximide blocked Abeta(25-35)-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 Abeta-induced activation of endozepine biosynthesis and release may contribute to astrocyte proliferation associated with Alzheimer's disease.[1]


  1. Beta-amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes. Tokay, T., Masmoudi, O., Gandolfo, P., Leprince, J., Pelletier, G., Vaudry, H., Tonon, M.C. J. Neurochem. (2005) [Pubmed]
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