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Aging-induced type I interferon response at the choroid plexus negatively affects brain function
Open accessAbstract
Excess signaling is bad for the aging brain: Preventing antiviral-like responses may protect function in the aging brain. Baruch et al. monitored messenger RNA production in the choroid plexus, the interface between the blood and cerebrospinal fluid, in young and old mice (see the Perspective by Ransohoff). They detected an inflammatory response in older mice not present in the brain of young mice that was also seen in old aged human samples postmortem. Preventing signaling by the cytokine interferon-I, which normally helps in the antiviral response of the immune system, helped prevent the decrease in cognitive function seen in aged mice. Science , this issue p. 89 ; see also p. 36
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“Astrocytes and microglia, mediators of the innate immune response of the central nervous system, become hyper-activated with age (Baruch et al., 2014; Norden and Godbout, 2013).”
From Loss of epigenetic information as a cause of mammalian aging (2023) · cites this paper as Baruch et al., 2014
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Recent findings from parabiosis models (left) have shown that exposure to young blood restores neurogenesis, learning and memory and neuronal functions in older mice via increase in growth factors and endothelial remodeling in older mice(Baruch et al, 2014;Katsimpardi et al, 2014;Villeda et al, 2011).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
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“In addition, it has been found that the level of IFN-γ was reduced at the CP of aging brain,148 indicating an attenuated ability to resolve inflammation in aging brain.”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [148]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The presence of a type I IFN signature in brain cells, in particular in microglia, is increasingly being associated with ageing and neurodegenerative disease in various species13,15,39,44–50.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [15]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Cells harboring PSMC5 variants exhibit characteristics reminiscent of senescent or neurodegenerative cells, including impaired mitophagy47, type I IFN response48, abnormal apolipoproteins and/or cholesterol levels49,50, cognitive inflexibility51,52, impaired neuritogenesis53,54, and an imbalanced E/I ratio55,56.”
From Investigating the neuronal role of the proteasomal ATPase subunit gene PSMC5 in neurodevelopmental proteasomopathies (2025) · cites this paper as [48]
In the citing paper
“The inflamed choroid plexus has previously been shown to send inflammatory signals into the brain, thereby activating parenchymal glia and impairing cognitive function31.”
From Dysregulation of brain and choroid plexus cell types in severe COVID-19 (2021) · cites this paper as [31]
In the citing paper
“so it is plausible that Cluster OA3 microglia also play a role in contributing to the inflammatory tone of the aged brain.”
From Complex cell-state changes revealed by single cell RNA sequencing of 76,149 microglia throughout the mouse lifespan and in the injured brain (2018) · cites this paper as Baruch et al., 2014
In the citing paper
“Although IFNγ can also have positive effects, IFNα has an overall negative impact on the brain137. Chronic inflammation and IFNα convert αNSCs into ΩNSCs, which are more quiescent138.”
From Ageing and rejuvenation of tissue stem cells and their niches (2023) · cites this paper as [137]
In the citing paper
“These were enriched for specialized programs across ages: Embryonic epithelia upregulated genes for developmental processes (Figure 3K, S3K), while aged epithelia upregulated host-defense programs (Figure 3L, FDR q-value < 0.01, GOrilla (Eden et al., 2007, 2009;Baruch et al., 2014).”
From A cellular and spatial map of the choroid plexus across brain ventricles and ages (2021) · cites this paper as Baruch et al., 2014
In the citing paper
“IL-1β expression was induced in aged ChP macrophages”
From A cellular and spatial map of the choroid plexus across brain ventricles and ages (2021) · cites this paper as Baruch et al., 2014
In the citing paper
“Overall, we observed an upregulation of the inflammatory signals in the aged ChP in agreement with prior studies (Baruch et al., 2014) that was reflected in expression of Ifit1 and Il1b in aged epithelial cells.”
From A cellular and spatial map of the choroid plexus across brain ventricles and ages (2021) · cites this paper as Baruch et al., 2014
In the citing paper
“Moreover, neutralizing antibodies against IFN-I restored growth factor levels and cognitive functioning in aged mice, thus demonstrating the role of blood-derived factors in aging-induced neurological deficits (Baruch et al, 2014).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
In the citing paper
“Indeed, gene expression analysis of the choroid plexus, a brain region marked by epithelial lining that serves as a neurovascular interface, revealed an aging-induced upregulation of interferon-I (IFN-I) and downregulation of interferon-II response genes (Baruch et al, 2014).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
In the citing paper
“Recent findings from parabiosis models (left) have shown that exposure to young blood restores neurogenesis, learning and memory and neuronal functions in older mice via increase in growth factors and endothelial remodeling in older mice(Baruch et al, 2014;Katsimpardi et al, 2014;Villeda et al, 2011).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
In the citing paper
“Recent findings from parabiosis models (left) have shown that exposure to young blood restores neurogenesis, learning and memory and neuronal functions in older mice via increase in growth factors and endothelial remodeling in older mice(Baruch et al, 2014;Katsimpardi et al, 2014;Villeda et al, 2011).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
In the citing paper
“Recent findings from parabiosis models (left) have shown that exposure to young blood restores neurogenesis, learning and memory and neuronal functions in older mice via increase in growth factors and endothelial remodeling in older mice(Baruch et al, 2014;Katsimpardi et al, 2014;Villeda et al, 2011).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Baruch et al, 2014
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Metadata
- Authors
- Baruch, K., Deczkowska, A., David, E., Castellano, J. M., Miller, O., Kertser, A., Berkutzki, T., Barnett-Itzhaki, Z., Bezalel, D., Wyss-Coray, T., Amit, I., & Schwartz, M.
- Affiliations
- Weizmann Institute of Science (IL)
- Stanford Medicine (US)
- Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
- Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
- Corresponding author
- Baruch, Kuti
- Deczkowska, Aleksandra
- Amit, Ido
- Schwartz, Michal
- ORCID
- Venue
- Science
- Published
- 2014-10-03
- Volume
- 346
- Issue
- 6205
- Pages
- 89-93
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4869326
- OpenAlex
- W2061769617
- Cited by
- 615
- References
- 44
- Citations by year
- 2026: 52 · 2025: 47 · 2024: 58 · 2023: 64 · 2022: 69 · 2021: 60 · 2020: 60 · 2019: 56 · 2018: 32 · 2017: 28 · 2016: 47 · 2015: 37 · 2014: 5
- FWCI
- 20.25
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Medical Research Council (MR/L022656/1)
- National Institute on Aging (AG045034, R01AG045034)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- aging, type I interferon, choroid plexus, cognitive decline, cerebrospinal fluid, hippocampal neurogenesis, antiviral response, brain aging, aged mice
- MeSH terms
- Interferon gamma Receptor, Aging, Animals, Brain, Choroid Plexus, Cognition, Gene Expression Regulation, Hippocampus, Interferon Type I, Mice, Transgenic, Receptors, Interferon, Interferon Regulatory Factors, Mice, Neurogenesis
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