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    Old maids: Aging and its impact on microglia function

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    Author
    Koellhoffer, E.C.
    McCullough, L.D.
    Ritzel, R.M.
    Date
    2017
    Journal
    International Journal of Molecular Sciences
    Publisher
    MDPI AG
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://www.doi.org/10.3390/ijms18040769
    Abstract
    Microglia are highly active and vigilant housekeepers of the central nervous system that function to promote neuronal growth and activity. With advanced age, however, dysregulated inflammatory signaling and defects in phagocytosis impede their ability to perform the most essential of homeostatic functions, including immune surveillance and debris clearance. Microglial activation is one of the hallmarks of the aging brain and coincides with age-related neurodegeneration and cognitive decline. Age-associated microglial dysfunction leads to cellular senescence and can profoundly alter the response to sterile injuries and immune diseases, often resulting in maladaptive responses, chronic inflammation, and worsened outcomes after injury. Our knowledge of microglia aging and the factors that regulate age-related microglial dysfunction remain limited, as the majority of pre-clinical studies are performed in young animals, and human brain samples are difficult to obtain quickly post-mortem or in large numbers. This review outlines the impact of normal aging on microglial function, highlights the potential mechanisms underlying age-related changes in microglia, and discusses how aging can shape the recovery process following injury. Copyright 2017 by the authors. Licensee MDPI, Basel, Switzerland.
    Sponsors
    This work was supported by National Institutes of Health grants R01 NS094543 (Louise D. McCullough), F31 NS083244 (Rodney M. Ritzel), and F30 NS095511 (Edward Koellhoffer).
    Keyword
    Aging
    Dysregulation
    Inflammation
    Microglia
    Senescence
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85017260010&doi=10.3390%2fijms18040769&partnerID=40&md5=f8d6837c2b295ed6bc756cfe4cde2578; http://hdl.handle.net/10713/9947
    ae974a485f413a2113503eed53cd6c53
    10.3390/ijms18040769
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