期刊
NATURE
卷 477, 期 7362, 页码 90-U157出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nature10357
关键词
-
资金
- Department of Veterans Affairs
- National Institutes of Health Institute on Aging [R01 AG027505, P30AG08017]
- California Initiative for Regenerative Medicine
- National Institutes of Health [R01 MH078194]
- Larry L. Hillblom Foundation [2008-A-023-FEL]
- Feodor-Lynen postdoctoral fellowship
- Swiss National Science Foundation
- National Science Foundation
- Kirschstein NRSA [AG034045-01, 1 F31 NS066676-01A1]
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(1). Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise(1). 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据