Frailty and sarcopenia: The potential role of an aged immune system

Research output: Contribution to journalArticle

Colleges, School and Institutes

External organisations

  • MRC-ARUK Centre for Musculoskeletal Ageing Research, Institute of Inflammation and Ageing, University of Birmingham, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WD, UK. Electronic address: d.v.wilson@bham.ac.uk.
  • MRC-ARUK Centre for Musculoskeletal Ageing Research, Institute of Inflammation and Ageing, University of Birmingham, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WD, UK.

Abstract

Frailty is a common negative consequence of ageing. Sarcopenia, the syndrome of loss of muscle mass, quality and strength, is more common in older adults and has been considered a precursor syndrome or the physical manifestation of frailty. The pathophysiology of both syndromes is incompletely described with multiple causes, inter-relationships and complex pathways proposed. Age-associated changes to the immune system (both immunesenescence, the decline in immune function with ageing, and inflammageing, a state of chronic inflammation) have been suggested as contributors to sarcopenia and frailty but a direct causative role remains to be established. Frailty, sarcopenia and immunesenescence are commonly described in older adults but are not ubiquitous to ageing. There is evidence that all three conditions are reversible and all three appear to share common inflammatory drivers. It is unclear whether frailty, sarcopenia and immunesenescence are separate entities that co-occur due to coincidental or potentially confounding factors, or whether they are more intimately linked by the same underlying cellular mechanisms. This review explores these possibilities focusing on innate immunity, and in particular associations with neutrophil dysfunction, inflammation and known mechanisms described to date. Furthermore, we consider whether the age-related decline in immune cell function (such as neutrophil migration), increased inflammation and the dysregulation of the phosphoinositide 3-kinase (PI3K)-Akt pathway in neutrophils could contribute pathogenically to sarcopenia and frailty.

Details

Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalAgeing Research Reviews
Volume36
Early online date20 Feb 2017
Publication statusPublished - Jul 2017

Keywords

  • Frailty, Inactivity, Immunesenescence, Inflammaging, Sarcopenia, Neutrophil