Smooth muscle cells cultured from amyloid-beta-affected arteries accumulate amyloid-beta peptide A beta. We now show that accumulation of "A beta" deposits in this model can be significantly reduced by culture in conditioned media from microglia and monocytes. Reduced A beta accumulation was associated with (i) lower secretion of A beta, (ii) increased secretion, but not cellular levels of amyloid-beta-precursor protein (A beta PP), and (iii) increased cell proliferation and metabolic activity. We suggest that improper regulation of A beta PP metabolism by monokines may facilitate vascular amyloidogenesis.
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