| Literature DB >> 23792036 |
Martin Michaud1, Laurent Balardy, Guillaume Moulis, Clement Gaudin, Caroline Peyrot, Bruno Vellas, Matteo Cesari, Fati Nourhashemi.
Abstract
Inflammation is a physiological process that repairs tissues in response to endogenous or exogenous aggressions. Nevertheless, a chronic state of inflammation may have detrimental consequences. Aging is associated with increased levels of circulating cytokines and proinflammatory markers. Aged-related changes in the immune system, known as immunosenescence, and increased secretion of cytokines by adipose tissue, represent the major causes of chronic inflammation. This phenomenon is known as "inflamm-aging." High levels of interleukin (IL)-6, IL-1, tumor necrosis factor-α, and C-reactive protein are associated in the older subject with increased risk of morbidity and mortality. In particular, cohort studies have indicated TNF-α and IL-6 levels as markers of frailty. The low-grade inflammation characterizing the aging process notably concurs at the pathophysiological mechanisms underlying sarcopenia. In addition, proinflammatory cytokines (through a variety of mechanisms, such as platelet activation and endothelial activation) may play a major role in the risk of cardiovascular events. Dysregulation of the inflammatory pathway may also affect the central nervous system and be involved in the pathophysiological mechanisms of neurodegenerative disorders (eg, Alzheimer disease).The aim of the present review was to summarize different targets of the activity of proinflammatory cytokines implicated in the risk of pathological aging.Entities:
Keywords: Alzheimer disease; Inflammation; Interleukin-6; TNF-α; aging; cytokines; frailty
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Year: 2013 PMID: 23792036 DOI: 10.1016/j.jamda.2013.05.009
Source DB: PubMed Journal: J Am Med Dir Assoc ISSN: 1525-8610 Impact factor: 4.669