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Fibril-enriched amyloid-β inhibits interleukin-1 induced expression of the transcription factor C/EBPδ in astrocytes but not in microglia
Stockholm University, Faculty of Science, Department of Neurochemistry.ORCID iD: 0000-0002-6668-1094
Stockholm University, Faculty of Science, Department of Neurochemistry.ORCID iD: 0000-0002-9065-9268
Stockholm University, Faculty of Science, Department of Neurochemistry.ORCID iD: 0000-0002-1007-747X
Stockholm University, Faculty of Science, Department of Neurochemistry.
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(English)Manuscript (preprint) (Other academic)
National Category
Biological Sciences Chemical Sciences
Research subject
Neurochemistry with Molecular Neurobiology
Identifiers
URN: urn:nbn:se:su:diva-95102OAI: oai:DiVA.org:su-95102DiVA: diva2:658293
Available from: 2013-10-21 Created: 2013-10-21 Last updated: 2016-01-29Bibliographically approved
In thesis
1. Neuroinflammation in Alzheimer’s disease and obesity
Open this publication in new window or tab >>Neuroinflammation in Alzheimer’s disease and obesity
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Alzheimer’s disease (AD) and obesity are both major problems in the western world. Although they may appear to have little in common at first glance, they are both characterized by chronic inflammation. Exactly how inflammation affects these disorders is far from clear. Microglia, the resident immune cells of the brain, can take on different phenotypes in response to inflammatory stimuli. They can become classically or alternatively activated, where they secrete pro- or anti-inflammatory cytokines respectively. The inflammatory response is to a large part regulated by transcription factors, such as C/EBPδ, which regulate gene expression. The aim of this thesis was to investigate 1) effects of the Alzheimer’s related peptide amyloid-β (Aβ) on C/EBPδ in astrocytes and microglia during inflammatory conditions, 2) how microglia is affected by elevated levels of free fatty acids (FFAs) occurring in obesity and 3) possible cellular sources of the neuroprotective peptide GLP-1 in the brain. In paper I we found that IL-1β-induced C/EBPδ appears to be blocked by Aβ fibrils but not Aβ oligomers in mixed glial cells. In paper II we found that the decreased levels of C/EBPδ were limited to astrocytes under inflammatory conditions and that there was no blocking of IL-1β-induced C/EBPδ in microglia. In paper III we found that the FFA palmitate induces an alternative activation in microglia with no effect on the expression of C/EBPδ or the pro-inflammatory cytokines TNF-α, IL-1β and IL-6. However, pre-exposure to palmitate potentiated microglia phagocytosis and changed the mRNA expression profile of some pro-inflammatory cytokines in response to inflammatory stimuli. In paper IV we found microglia to be a novel source of secreted GLP-1. Further, we found that the GLP-1 secretion could be decreased by inflammatory stimuli. In summary, the inflammatory response of C/EBPδ in AD appears to be disturbed. In addition, palmitate affects the response to inflammatory stimuli in microglia.

Place, publisher, year, edition, pages
Stockholm: Department of Neurochemistry, Stockholm University, 2013. 56 p.
Keyword
Alzheimer's disease, obesity, neuroinflammation
National Category
Natural Sciences
Research subject
Neurochemistry with Molecular Neurobiology
Identifiers
urn:nbn:se:su:diva-95104 (URN)978-91-7447-731-3 (ISBN)
Public defence
2013-11-22, Magnélisalen, Kemiska övningslaboratoriet, Svante Arrhenius väg 16 B, Stockholm, 13:00 (English)
Opponent
Supervisors
Note

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript.

Available from: 2013-10-31 Created: 2013-10-21 Last updated: 2015-03-16Bibliographically approved

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