期刊
ELIFE
卷 9, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.54083
关键词
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类别
资金
- Alzheimer Forschung Initiative [18014]
- Deutsche Forschungsgemeinschaft [EXC 2145 SyNergy, 390857198, HA1737/16-1]
- H2020 European Research Council [ERC-StG 802305]
- Helmholtz-Gemeinschaft [ZT-0027]
- Bundesministerium fur Bildung und Forschung JPND PMG-AD
- Bundesministerium fur Bildung und Forschung CLINSPECT-M
- NCL Foundation [01133]
Microglial dysfunction is a key pathological feature of Alzheimer's disease (AD), but little is known about proteome-wide changes in microglia during the course of AD and their functional consequences. Here, we performed an in-depth and time-resolved proteomic characterization of microglia in two mouse models of amyloid beta (A beta) pathology, the overexpression APPPS1 and the knock-in APP-NL-G-F (APP-KI) model. We identified a large panel of Microglial A beta Response Proteins (MARPs) that reflect heterogeneity of microglial alterations during early, middle and advanced stages of A beta deposition and occur earlier in the APPPS1 mice. Strikingly, the kinetic differences in proteomic profiles correlated with the presence of fibrillar A beta, rather than dystrophic neurites, suggesting that fibrillar A beta may trigger the AD-associated microglial phenotype and the observed functional decline. The identified microglial proteomic fingerprints of AD provide a valuable resource for functional studies of novel molecular targets and potential biomarkers for monitoring AD progression or therapeutic efficacy.
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