期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep30028
关键词
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资金
- Cure Alzheimer's Fund (CAF)
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [DK42086]
Severe amyloidosis and plaque-localized neuro-inflammation are key pathological features of Alzheimer's disease (AD). In addition to astrocyte and microglial reactivity, emerging evidence suggests a role of gut microbiota in regulating innate immunity and influencing brain function. Here, we examine the role of the host microbiome in regulating amyloidosis in the APPSWE/PS1.E9 mouse model of AD. We show that prolonged shifts in gut microbial composition and diversity induced by long-term broadspectrum combinatorial antibiotic treatment regime decreases A beta plaque deposition. We also show that levels of soluble A beta are elevated and that levels of circulating cytokine and chemokine signatures are altered in this setting. Finally, we observe attenuated plaque-localised glial reactivity in these mice and significantly altered microglial morphology. These findings suggest the gut microbiota community diversity can regulate host innate immunity mechanisms that impact A beta amyloidosis.
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