Cited by 620Neuroinflammation and Neurodegeneration Mechanismsinterferon and immune responsesGenetics, Aging, and Longevity in Model Organisms

Aging-induced type I interferon response at the choroid plexus negatively affects brain function

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Baruch, Kuti, Deczkowska, Aleksandra, David, Eyal, Castellano, Joseph M., Miller, Omer, Kertser, Alexander, Berkutzki, Tamara, Barnett-Itzhaki, Zohar +4 more·2014·Science

Abstract

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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Crossref · 10.1126/science.1252945

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  • Astrocytes and microglia become hyper-activated with age.

    “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

    The passage discussing Fig. 4F–G reports that blocking IFN-I in aged mice markedly decreased astrogliosis and microgliosis, which the authors describe as age-related neuroinflammation. This supports glial activation in aged mice, but the cited passage does not directly show that astrocyte and microglial activation increases from young to old age. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • The level of IFN-γ is reduced at the choroid plexus of aging brain, indicating an attenuated ability to resolve inflammation in aging brain.

    “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]

    The paper reports diminished IFN-II (IFN-γ) at the aging choroid plexus and decreased expression of IFN-γ-dependent genes there (section labelled Abstract; no page given). It does not establish that the aging brain has an attenuated ability to resolve inflammation; it cites evidence about IFN-II-dependent resolution in other inflammatory conditions. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • Presence of a type I IFN signature in brain cells, in particular microglia, is increasingly associated with ageing and neurodegenerative disease in various species.

    “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]

    The Abstract reports an age-associated type I IFN signature at the choroid plexus in mice and humans. It does not establish that the signature is present particularly in microglia or associate a microglial signature with neurodegenerative disease; its microgliosis finding concerns the effect of blocking IFN-I in aged mice. No page number is provided in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Cells harboring PSMC5 variants exhibit characteristics reminiscent of senescent or neurodegenerative cells.

    “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.”
  • The inflamed choroid plexus sends inflammatory signals into the brain, activating parenchymal glia and impairing cognitive function.

    “The inflamed choroid plexus has previously been shown to send inflammatory signals into the brain, thereby activating parenchymal glia and impairing cognitive function31.”

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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
Venue
Science
Published
2014-10-03
Volume
346
Issue
6205
Pages
89-93
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
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
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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