Villeda · Nature 2011 · controlled animal experiment and human cross-sectional biomarker study · n=?

The ageing systemic milieu negatively regulates neurogenesis and cognitive function.

Cited 1795 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Animal experimental research with correlational human fluid biomarker profiling.

PubMed 21886162 · doi:10.1038/nature10357 · record verified 2026-08-26

What was done

Researchers evaluated the impact of the aging systemic milieu on adult neural stem/progenitor cells, neurogenesis, synaptic plasticity, and cognitive function (contextual fear conditioning and spatial learning/memory) in mice using heterochronic parabiosis and plasma transfers. They screened for systemic factors associated with neurogenesis decline, quantified CCL11 (eotaxin) in plasma and cerebrospinal fluid from healthy aging humans, and tested the effects of systemic CCL11 administration on neurogenesis and cognition in young mice.

What was found

The abstract reports no numerical values, sample sizes, or effect sizes. Exposing young mice to an aged systemic environment or old plasma decreased synaptic plasticity, adult neurogenesis, and cognitive performance in contextual fear conditioning and spatial learning and memory. CCL11 levels correlated with reduced neurogenesis in mice and were increased in human plasma and cerebrospinal fluid with age. Systemic CCL11 administration in young mice decreased adult neurogenesis and impaired learning and memory.

Why it matters

The study shows that systemic blood-borne factors actively drive aspects of brain aging and cognitive decline, identifying circulating molecules such as CCL11 as potential targets for interventions targeting brain aging.

Limits

The abstract provides no sample sizes, numerical data, or statistical effect estimates for animal or human experiments. Mechanistic and cognitive findings are derived from rodent models, and human evidence is limited to correlational biomarker levels across aging.

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