Uptake, degradation, and release of fibrillar and soluble forms of Alzheimer's amyloid β-peptide by microglial cells Academic Article uri icon

Overview

MeSH Major

  • Fractures, Compression
  • Lumbar Vertebrae
  • Spinal Fractures
  • Thoracic Vertebrae

abstract

  • Microglia are phagocytic cells that are the main inflammatory response cells of the central nervous system. In Alzheimer's disease brain, activated microglia are concentrated in regions of compact amyloid deposits that contain the 39-43-amino acid Abeta peptide. We examined the uptake, degradation, and release of small aggregates of fibrillar Abeta (fAbeta) or soluble Abeta (sAbeta) by microglia. We found that although some degradation of fAbeta was observed over 3 days, no further degradation was observed over the next 9 days. Instead, there was a slow release of intact Abeta. The poor degradation was not due to inhibition of lysosomal function, since the rate of alpha2-macroglobulin degradation was not affected by the presence of fAbeta in the late endosomes/lysosomes. In contrast to fAbeta, internalization of sAbeta was not saturable. After internalization, sAbeta was released rapidly from microglia, and very little was degraded. These data show that fAbeta and sAbeta interact differently with microglia but that after internalization a large fraction of both are released without degradation.

publication date

  • November 5, 1999

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1074/jbc.274.45.32301

Additional Document Info

start page

  • 32301

end page

  • 8

volume

  • 274

number

  • 45