Factors produced by activated macrophages reduce accumulation of Alzheimer's beta-amyloid protein in vascular smooth muscle cells

Brain Res. 1997 Jun 20;760(1-2):255-60. doi: 10.1016/s0006-8993(97)00327-2.

Abstract

Smooth muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellularly amyloid-beta peptide (A beta). Now we demonstrate that accumulation of A beta in SMCs can be reduced by factors secreted by macrophages - IL-1alpha, IL-6, TNF-alpha, TGF-beta1 or PGE2 - probably by stimulating the non-amyloidogenic processing of A beta precursor protein (PP). It is suggested that brain macrophages may regulate A betaPP/A beta metabolism under physiological conditions and prevent beta-amyloidosis. The disturbance of this regulatory function of brain macrophages may result in excessive production and accumulation of A beta.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amyloid beta-Protein Precursor / drug effects
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Brain / metabolism
  • Cattle
  • Dogs
  • Immunohistochemistry
  • Interleukin-1 / pharmacology
  • Interleukin-6 / pharmacology
  • Macrophages / metabolism*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Amyloid beta-Protein Precursor
  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha