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Anti-inflammatory (M2) macrophage media reduce transmission of oligomeric amyloid beta in differentiated SH-SY5Y cells
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi.
Karolinska Hospital Solna, Sweden.
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2017 (engelsk)Inngår i: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 60, s. 173-182Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Neuroinflammation plays an influential role in Alzheimers 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.

sted, utgiver, år, opplag, sider
ELSEVIER SCIENCE INC , 2017. Vol. 60, s. 173-182
Emneord [en]
Anti-inflammatory; Proinflammatory; Amyloid beta oligomers; Cytokine; Cell-to-cell transfer; Alzheimers disease
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Identifikatorer
URN: urn:nbn:se:liu:diva-143067DOI: 10.1016/j.neurobiolaging.2017.08.022ISI: 000414424800016PubMedID: 28969867OAI: oai:DiVA.org:liu-143067DiVA, id: diva2:1158441
Merknad

Funding Agencies|Swedish Research Council [523-2013-2735]; Swedish Alzheimer foundation; Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research; Gustav V and Queen Victorias Foundation; Swedish Dementia Foundation; Linkoping University Neurobiology Centre; County Council of Ostergotland

Tilgjengelig fra: 2017-11-20 Laget: 2017-11-20 Sist oppdatert: 2018-05-03

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Sackmann, ValerieAnsell - Schultz, AnnaSackmann, ChristopherHallbeck, MartinNilsberth, Camilla
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