Journal
SCIENCE
Volume 346, Issue 6205, Pages 89-93Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1252945
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Funding
- European Research Council (E.R.C.) [232835]
- European Union [279017, 309788]
- Israeli Science Foundation [1782/11]
- National Institute on Aging [AG045034]
- Jane Coffin Childs Postdoctoral fellowship
- Medical Research Council [MR/L022656/1] Funding Source: researchfish
- MRC [MR/L022656/1] Funding Source: UKRI
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Aging-associated cognitive decline is affected by factors produced inside and outside the brain. By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interface between the brain and the circulation, shows a type I interferon (IFN-I)-dependent gene expression profile that was also found in aged human brains. In aged mice, this response was induced by brain-derived signals, present in the cerebrospinal fluid. Blocking IFN-I signaling within the aged brain partially restored cognitive function and hippocampal neurogenesis and reestablished IFN-II-dependent choroid plexus activity, which is lost in aging. Our data identify a chronic aging-induced IFN-I signature, often associated with antiviral response, at the brain's choroid plexus and demonstrate its negative influence on brain function, thereby suggesting a target for ameliorating cognitive decline in aging.
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