Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Amyloid-beta uptake by blood monocytes is reduced with ageing and Alzheimer's disease.

Abstract

Deficits in the clearance of amyloid beta-protein (Abeta) play a pivotal role in the pathogenesis of sporadic Alzheimer's disease (AD). The roles of blood monocytes in the development of AD remain unclear. In this study, we sought to investigate the alterations in the Abeta phagocytosis function of peripheral monocytes during ageing and in AD patients. A total of 104 cognitively normal participants aged 22-89 years, 24 AD patients, 25 age- and sex-matched cognitively normal (CN) subjects, 15 Parkinson's disease patients (PD), and 15 age- and sex-matched CN subjects were recruited. The Abeta uptake by blood monocytes was measured and its alteration during ageing and in AD patients were investigated. Abeta1-42 uptake by monocytes decreased during ageing and further decreased in AD but not in PD patients. Abeta1-42 uptake by monocytes was associated with Abeta1-42 levels in the blood. Among the Abeta uptake-related receptors and enzymes, the expression of Toll-like receptor 2 (TLR2) was reduced in monocytes from AD patients. Our findings suggest that monocytes regulate the blood levels of Abeta and might be involved in the development of AD. The recovery of the Abeta uptake function by blood monocytes represents a potential therapeutic strategy for AD.