In the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions. 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.
Friday, October 21, 2011
The brain's fountain of youth
Williams points to an article that suggests that Dracula may have gotten it right. Young blood can restore an aging body. Giving young blood to older mice is know to boost their immune system and muscle function, and now it turns out that it also causes the synthesis of new nerve cells, boosting the number of cells in the hippocampus involved in memory formation. Conversely, serum from older mice decreases the number of these memory cells in younger mice. Wyss-Coray and collaborators find a blood borne protein (cytokine CCL11) that increases with aging and inhibits synthesis of new nerve cells. Factors stimulating neurogenesis are being sought. Here is their abstract: