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      The aging systemic milieu negatively regulates neurogenesis and cognitive function

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          In the central nervous system (CNS), aging results in a precipitous decline in adult neural stem/progenitor cells (NPCs) 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 animal 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/Eotaxin – whose plasma levels correlate with reduced neurogenesis in heterochronic parabionts and aged mice, and whose levels are increased in plasma and cerebral spinal fluid of healthy aging humans. Finally, 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 aging can be in part attributed to changes in blood-borne factors.

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          Most cited references 35

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          A synaptic model of memory: long-term potentiation in the hippocampus.

          Long-term potentiation of synaptic transmission in the hippocampus is the primary experimental model for investigating the synaptic basis of learning and memory in vertebrates. The best understood form of long-term potentiation is induced by the activation of the N-methyl-D-aspartate receptor complex. This subtype of glutamate receptor endows long-term potentiation with Hebbian characteristics, and allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and postsynaptic mechanisms to generate a persistent increase in synaptic strength.
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            Mammalian neural stem cells.

             Brian F Gage (2000)
            Neural stem cells exist not only in the developing mammalian nervous system but also in the adult nervous system of all mammalian organisms, including humans. Neural stem cells can also be derived from more primitive embryonic stem cells. The location of the adult stem cells and the brain regions to which their progeny migrate in order to differentiate remain unresolved, although the number of viable locations is limited in the adult. The mechanisms that regulate endogenous stem cells are poorly understood. Potential uses of stem cells in repair include transplantation to repair missing cells and the activation of endogenous cells to provide "self-repair. " Before the full potential of neural stem cells can be realized, we need to learn what controls their proliferation, as well as the various pathways of differentiation available to their daughter cells.
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              Mechanisms and functional implications of adult neurogenesis.

              The generation of new neurons is sustained throughout adulthood in the mammalian brain due to the proliferation and differentiation of adult neural stem cells. In this review, we discuss the factors that regulate proliferation and fate determination of adult neural stem cells and describe recent studies concerning the integration of newborn neurons into the existing neural circuitry. We further address the potential significance of adult neurogenesis in memory, depression, and neurodegenerative disorders such as Alzheimer's and Parkinson's disease.
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                Author and article information

                Journal
                0410462
                6011
                Nature
                Nature
                Nature
                0028-0836
                1476-4687
                1 August 2011
                31 August 2011
                01 March 2012
                : 477
                : 7362
                : 90-94
                Affiliations
                [1 ]Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
                [2 ]Neuroscience IDP Program, Stanford University School of Medicine, Stanford, California 94305, USA
                [3 ]AfaSci Research Laboratory, Redwood City, California, 94063, USA
                [4 ]School of Life Sciences, Swiss Federal Institute of Technology (EPFL), CH-1015 Lausanne, Switzerland
                [5 ]Immunology IDP Program, Stanford University School of Medicine, Stanford, California 94305, USA
                [6 ]Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, A-5020 Salzburg, Austria
                [7 ]Dept. of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA 98108-1597, USA
                [8 ]Veterans Affairs Northwest Network Mental Illness Research, Education, and Clinical Center, Seattle, WA 98108-1597, USA
                [9 ]Layton Aging & Alzheimer’s Disease Center, Oregon Health and Science University, CR131, 3181 SW Sam Jackson Park Road, Portland, OR 97201-3098, USA and Portland VA Medical Center, Portland, OR 97207
                [10 ]Department of Neurosciences, University of California San Diego, 9500 Gilman Drive #0948, La Jolla, CA 92093-0948, USA
                [11 ]Center for Tissue Regeneration, Repair and Restoration, VA Palo Alto Health Care System, Palo Alto, California 94304, USA
                [12 ]The Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA 94305, USA
                Author notes
                [* ]Corresponding Author: twc@ 123456stanford.edu
                [#]

                Current address: CNS Discovery, pRED, F. Hoffmann-La Roche Ltd., Basel, Switzerland

                Article
                nihpa313001
                10.1038/nature10357
                3170097
                21886162

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                Funding
                Funded by: National Institute on Aging : NIA
                Award ID: R01 AG027505-05 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: R01 AG027505-04 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: R01 AG027505-03 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: R01 AG027505-02 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: R01 AG027505-01A1 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: F31 AG034045-03 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: F31 AG034045-02 || AG
                Funded by: National Institute on Aging : NIA
                Award ID: F31 AG034045-01 || AG
                Funded by: Office of the Director : NIH
                Award ID: DP1 OD000392-05 || OD
                Funded by: Office of the Director : NIH
                Award ID: DP1 OD000392-04 || OD
                Funded by: Office of the Director : NIH
                Award ID: DP1 OD000392-03 || OD
                Funded by: Office of the Director : NIH
                Award ID: DP1 OD000392-02 || OD
                Funded by: Office of the Director : NIH
                Award ID: DP1 OD000392-01 || OD
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