The Ageing Systemic Milieu Negatively Regulates Neurogenesis and Cognitive Function

dc.contributor.authorVilleda,Saul.A
dc.contributor.authorLuo, Jian
dc.contributor.authorBieri, Gregor
dc.contributor.authorKaye, Jeffrey A.
dc.contributor.authorRando,Thomas A.
dc.date.accessioned2024-12-13T17:25:06Z
dc.date.available2024-12-13T17:25:06Z
dc.date.issued2011-08-31
dc.description.abstractIn the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions1. Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise1. Here, using heterochronic parabiosis we show that blood-borne factors present in the systemic milieu can inhibit or promote adult neurogenesis in an age-dependent fashion in mice. Accordingly, exposing a young mouse to an old systemic environment or to plasma from old mice decreased synaptic plasticity, and impaired contextual fear conditioning and spatial learning and memory. We identify chemokines—including CCL11 (also known as eotaxin)—the plasma levels of which correlate with reduced neurogenesis in heterochronic parabionts and aged mice, and the levels of which are increased in the plasma and cerebrospinal fluid of healthy ageing humans. Lastly, increasing peripheral CCL11 chemokine levels in vivo in young mice decreased adult neurogenesis and impaired learning and memory. Together our data indicate that the decline in neurogenesis and cognitive impairments observed during ageing can be in part attributed to changes in blood-borne factors.
dc.identifier.citationVilleda, S., Luo, J., Mosher, K. et al. The ageing systemic milieu negatively regulates neurogenesis and cognitive function. Nature 477, 90–94 (2011). https://doi.org/10.1038/nature10357
dc.identifier.issn1476-4687
dc.identifier.urihttps://nru.uncst.go.ug/handle/123456789/9720
dc.language.isoes
dc.publisherNature
dc.titleThe Ageing Systemic Milieu Negatively Regulates Neurogenesis and Cognitive Function
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