000194998 001__ 194998
000194998 005__ 20250127125002.0
000194998 037__ $$aDZNE-2023-00181
000194998 041__ $$aEnglish
000194998 1001_ $$0P:(DE-2719)2810938$$aMüller, Stephan A$$b0$$eCorresponding author
000194998 245__ $$aDataset: Beneficial effect of ACI-24 vaccination on microglial phenotypes in an amyloidosis mouse model
000194998 260__ $$bPRoteomics IDEntifications Database$$c2023
000194998 3367_ $$2BibTeX$$aMISC
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000194998 3367_ $$2DINI$$aResearchData
000194998 520__ $$aAmyloid-beta (Aβ) deposition is an initiating factor in Alzheimer´s disease (AD). Microglia are the brain immune cells that surround and phagocytose Aβ, but their phagocytic capacity declines in AD. This is in agreement with studies that associate AD risk loci with genes regulating phagocytic function. Immunotherapies are currently pursued as therapeutic strategies against AD and there are increased efforts to understand the role of the immune system in ameliorating AD pathology. Here, we evaluated the effect of the Aβ targeting ACI-24 vaccine in preventing the AD pathology in an amyloidosis mouse model. ACI-24 vaccination elicited a robust and sustained antibody response in APPPS1 mice with an accompanying reduction of Aβ plaque load, amyloid plaque-associated ApoE and dystrophic neurites as compared to non-vaccinated controls. Furthermore, plaque-associated microglia had the tendency to be more activated post vaccination. The lower Aβ plaque load triggered by vaccination with ACI-24 was in concordance with the bulk transcriptomic analysis that revealed a reduction in the expression of several disease-associated microglial signatures. Accordingly, plaque-distant microglia displayed a more ramified morphology, supporting beneficial effects of the vaccination on bulk microglial phenotypes. Our study demonstrates that administration of the Aβ targeting vaccine, ACI-24, triggers protective microglial responses that translate into a reduction of AD pathology suggesting its use as a safe and cost effective AD therapeutic intervention.
000194998 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000194998 7001_ $$0P:(DE-2719)2181459$$aLichtenthaler, Stefan F$$b1$$eCorresponding author
000194998 7870_ $$0DZNE-2023-00136$$aNjavro, Jasenka et.al.$$dBasel : MDPI, 2022$$iRelatedTo$$r$$tBeneficial Effect of ACI-24 Vaccination on Aβ Plaque Pathology and Microglial Phenotypes in an Amyloidosis Mouse Model.
000194998 8564_ $$uhttps://www.ebi.ac.uk/pride/archive/projects/PXD038665
000194998 909CO $$ooai:pub.dzne.de:194998$$pVDB
000194998 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810938$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000194998 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2181459$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000194998 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000194998 9141_ $$y2023
000194998 9201_ $$0I:(DE-2719)1110006$$kAG Lichtenthaler$$lNeuroproteomics$$x0
000194998 980__ $$adataset
000194998 980__ $$aVDB
000194998 980__ $$aI:(DE-2719)1110006
000194998 980__ $$aUNRESTRICTED