Non-Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock


Real-time in vivo imaging reveals the ability of monocytes to clear vascular amyloid beta.


Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Abeta) that is assumed to result from impaired elimination of this neurotoxic peptide. Most patients with AD also exhibit cerebral amyloid angiopathy, which consists of Abeta deposition within the cerebral vasculature. The contribution of monocytes in AD has so far been limited to macrophage precursors. In this study, we aimed to investigate whether circulating monocytes could play a role in the elimination of Abeta. With live intravital two-photon microscopy, we demonstrate that patrolling monocytes are attracted to and crawl onto the luminal walls of Abeta-positive veins, but not on Abeta-positive arteries or Abeta-free blood vessels. Additionally, we report the presence of crawling monocytes carrying Abeta in veins and their ability to circulate back into the bloodstream. Selective removal of Ly6C(lo) monocytes in APP/PS1 mice induced a significant increase of Abeta load in the cortex and hippocampus. These data uncover the ability of Ly6C(lo) monocytes to naturally target and eliminate Abeta within the lumen of veins and constitute a potential therapeutic target in AD.

Authors: Michaud JP, Bellavance MA, Préfontaine P, Rivest S
Journal: Cell Rep; 2013 Nov 14; 5(3) 646-53. doi:10.1016/j.celrep.2013.10.010
Year: 2013
PubMed: PMID: 24210819 (Go to PubMed)