Abstract
By using the immortalized microglial cell line BV-2, we show that the high expression of theβA4 amyloid precursor protein (APP), its biogenesis and metabolism is modulated by TGF β, a cytokine with immunosuppressive activity, and by the microglia-stimulating agent LPS. TGFβ induces accumulation of cellular mature APP, the putative precursor of the amyloid subunit of Alzheimer's disease. LPS leads to an increase in cellular immature, non-amyloidogenic APP and secretion of also non-amyloidogenic APP fragments. We also demonstrate a functional involvement of ECM molecules in the regulation of microglial APP expression at mRNA and protein level by TGFβ and LPS.
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