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Updated: Feb 14, 2026

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Normal aging induces A1-like astrocyte reactivity.

Laura E Clarke1, Shane A Liddelow2,3,4, Chandrani Chakraborty2

  • 1Department of Neurobiology, Stanford University, School of Medicine, Stanford, CA 94305; lclarke2@stanford.edu.

Proceedings of the National Academy of Sciences of the United States of America
|February 14, 2018
PubMed
Summary
This summary is machine-generated.

Aging impairs astrocyte function, leading to a reactive A1-like phenotype. This astrocyte dysfunction, promoted by microglia, may drive cognitive decline and increase brain vulnerability in aged individuals.

Keywords:
RNA sequencingagingastrocytescognitive declinemicroglia

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Area of Science:

  • Neuroscience
  • Aging Research
  • Astrocyte Biology

Background:

  • Cognitive decline is a hallmark of aging, but its underlying mechanisms remain unclear.
  • Astrocytes play critical roles in synaptic function, and their dysfunction is linked to various neurological diseases.
  • The potential contribution of astrocyte dysfunction to age-related cognitive decline warrants investigation.

Purpose of the Study:

  • To investigate age-related changes in astrocyte gene expression across different brain regions.
  • To determine if astrocytes adopt a reactive phenotype during aging and identify factors influencing this transformation.
  • To elucidate the role of microglia in astrocyte activation during the aging process.

Main Methods:

  • RNA sequencing of astrocytes from various mouse brain regions across the lifespan using the Bac-Trap method.
  • Validation of gene expression changes using fluorescence in situ hybridization and quantitative PCR.
  • Analysis of astrocyte reactivity in response to lipopolysaccharide (LPS) and in mice lacking specific microglial cytokines.

Main Results:

  • Astrocytes exhibit region-specific transcriptional profiles that change with age.
  • Aged astrocytes display an upregulation of genes associated with a neuroinflammatory A1-like reactive phenotype, particularly in the hippocampus and striatum.
  • Microglia-derived cytokines (IL-1α, TNF, C1q) promote aging-induced astrocyte activation, as evidenced by reduced reactivity in knockout mice.

Conclusions:

  • Aging induces a reactive A1-like phenotype in astrocytes, potentially contributing to cognitive decline in vulnerable brain regions.
  • Astrocyte dysfunction, driven by microglial activation, may underlie age-related cognitive impairments.
  • The loss of normal astrocyte functions and neurotoxic effects of reactive astrocytes exacerbate brain vulnerability in aging.