期刊
NEUROBIOLOGY OF AGING
卷 60, 期 -, 页码 173-182出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2017.08.022
关键词
Anti-inflammatory; Proinflammatory; Amyloid beta oligomers; Cytokine; Cell-to-cell transfer; Alzheimer's disease
资金
- Swedish Research Council [523-2013-2735]
- Swedish Alzheimer foundation
- Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research
- Gustav V and Queen Victoria's Foundation
- Swedish Dementia Foundation
- Linkoping University Neurobiology Centre
- County Council of Ostergotland
Neuroinflammation plays an influential role in Alzheimer's disease (AD), although the mechanisms underlying this phenomenon remain largely unknown. Microglia are thought to be responsible for the majority of these effects and can be characterized into resting (M0), proinflammatory (M1), or anti-inflammatory (M2) functional phenotypes. We investigated the effects of conditioned macrophage media, as an analogue to microglia, on the transfer of oligomeric amyloid beta (oA beta) between differentiated SH-SY5Y cells. We also investigated how the different inflammatory environments related to intercellular and intracellular changes. We demonstrate that M2 products decrease interneuronal transfer of oA beta, while recombinant interleukin (IL)-4, IL-10, and IL-13 increase transfer. There were no alterations to the mRNA of a number of AD-related genes in response to the combination of oA beta and M0, M1, or M2, but several intracellular proteins, some relating to protein trafficking and the endosomal/lysosomal system, were altered. Stimulating microglia to an M2 phenotype may thus slow down the progression of AD and could be a target for future therapies. (C) 2017 Elsevier Inc. All rights reserved.
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