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Anti-inflammatory (M2) macrophage media reduce transmission of oligomeric amyloid beta in differentiated SH-SY5Y cells

Overview of attention for article published in Neurobiology of Aging, September 2017
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Title
Anti-inflammatory (M2) macrophage media reduce transmission of oligomeric amyloid beta in differentiated SH-SY5Y cells
Published in
Neurobiology of Aging, September 2017
DOI 10.1016/j.neurobiolaging.2017.08.022
Pubmed ID
Authors

Valerie Sackmann, Anna Ansell, Christopher Sackmann, Harald Lund, Robert A. Harris, Martin Hallbeck, Camilla Nilsberth

Abstract

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 (oAβ) 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 oAβ, 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 oAβ 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.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 15%
Student > Ph. D. Student 4 15%
Other 3 11%
Student > Bachelor 2 7%
Student > Master 2 7%
Other 4 15%
Unknown 8 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 19%
Neuroscience 4 15%
Pharmacology, Toxicology and Pharmaceutical Science 2 7%
Agricultural and Biological Sciences 2 7%
Medicine and Dentistry 2 7%
Other 2 7%
Unknown 10 37%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 04 January 2018.
All research outputs
#22,764,772
of 25,382,440 outputs
Outputs from Neurobiology of Aging
#4,224
of 4,418 outputs
Outputs of similar age
#284,752
of 324,453 outputs
Outputs of similar age from Neurobiology of Aging
#72
of 74 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,418 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 324,453 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 74 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.