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ApoE facilitates the microglial response to amyloid plaque pathology
Washington Univ, MO 63110 USA; Washington Univ, MO 63130 USA; Washington Univ, MO 63130 USA.
Washington Univ, MO 63130 USA.
Washington Univ, MO 63110 USA; Washington Univ, MO 63130 USA; Washington Univ, MO 63130 USA.
Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.ORCID iD: 0000-0002-4303-4783
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2018 (English)In: Journal of Experimental Medicine, ISSN 0022-1007, E-ISSN 1540-9538, Vol. 215, no 4, p. 1047-1058Article in journal (Refereed) Published
Abstract [en]

One of the hallmarks of Alzheimers disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-beta (A beta) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric A beta in the brain. In addition to influencing A beta metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1 Delta E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct A beta morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology.

Place, publisher, year, edition, pages
ROCKEFELLER UNIV PRESS , 2018. Vol. 215, no 4, p. 1047-1058
National Category
Immunology in the medical area
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URN: urn:nbn:se:liu:diva-150505DOI: 10.1084/jem.20171265ISI: 000440817800006PubMedID: 29483128OAI: oai:DiVA.org:liu-150505DiVA, id: diva2:1241656
Note

Funding Agencies|National Institutes of Health (NIH) [AG047644]; JPB Foundation; Cure Alzheimers Fund; NIH [RF1AG05148501, 5-T32CA009547-30]; New Vision Award through the Donors Cure Foundation [CCAD201703]; Lilly Innovation Fellowship from Eli Lilly and Company

Available from: 2018-08-24 Created: 2018-08-24 Last updated: 2019-11-08

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