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

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Aging brains show a type I interferon (IFN-I) signature in the choroid plexus, impacting cognitive function. Blocking this response partially restored cognition and brain health in aged mice.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Cognitive decline is a hallmark of aging, influenced by both internal and external factors.
  • The choroid plexus, a brain-circulatory interface, plays a crucial role in brain homeostasis.
  • Type I interferons (IFN-I) are typically associated with antiviral responses but are implicated in aging.

Purpose of the Study:

  • To investigate the role of the choroid plexus in aging-associated cognitive decline.
  • To identify molecular signatures in the aged choroid plexus and their impact on brain function.
  • To explore therapeutic strategies targeting IFN-I signaling for cognitive enhancement in aging.

Main Methods:

  • Multiorgan genome-wide analysis in aged mice.
  • Analysis of gene expression profiles in the choroid plexus.
  • Cerebrospinal fluid analysis to identify brain-derived signals.
  • Intervention by blocking IFN-I signaling in the aged brain.
  • Assessment of cognitive function and hippocampal neurogenesis.

Main Results:

  • Aged mice exhibit a type I interferon (IFN-I)-dependent gene expression profile in the choroid plexus, mirroring aged human brains.
  • This IFN-I signature is induced by brain-derived signals in the cerebrospinal fluid.
  • Blocking IFN-I signaling partially restored cognitive function and hippocampal neurogenesis.
  • Intervention reestablished IFN-II-dependent choroid plexus activity, which diminishes with age.

Conclusions:

  • A chronic, aging-induced IFN-I signature in the choroid plexus negatively impacts brain function and cognition.
  • Targeting IFN-I signaling in the brain presents a potential therapeutic strategy for mitigating age-related cognitive decline.