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Frailty and the role of inflammation, immunosenescence and cellular ageing in the very old: Cross-sectional findings from the Newcastle 85+ Study
Lookup NU author(s)
Dr Joanna Collerton
Dr Carmen Martin-Ruiz
karen Davies
Dr Catharien Hilkens
Professor John Isaacs
Claire Kolenda
Dr Craig Parker
Dr Michael Dunn
Professor Mike Catt
Professor Carol Jagger
Professor Thomas von Zglinicki
Professor Thomas Kirkwood CBE
Author(s)
Collerton J, Martin-Ruiz C, Davies K, Hilkens CM, Isaacs J, Kolenda C, Parker C, Dunn M, Catt M, Jagger C, von Zglinicki T, Kirkwood TB
Publication type
Article
Journal
Mechanisms of Ageing and Development
Year
2012
Volume
133
Issue
6
Pages
456-466
ISSN (print)
0047-6374
ISSN (electronic)
1872-6216
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Age-related frailty is an increasing societal challenge with growing emphasis on identifying its underlying pathophysiology and prospects for intervention. We report findings from the first comprehensive study of frailty and biomarkers of inflammation, immunosenescence and cellular ageing in the very old. Using cross-sectional data from the Newcastle 85+ Study (n=845, aged 85), frailty was operationalized by the Fried and Rockwood models and biomarker associations explored using regression analysis. We confirmed the importance of inflammatory markers (IL-6, TNF-alpha, CRP, neutrophils) in frailty in the very old, previously established only in younger-old populations. Limited evidence was found for immunosenescence in frailty; although total lymphocyte count was inversely related, no association was found with the immune risk profile and the inverse associations observed with memory/naive CD8 T and B cell ratios were in the opposite direction to that expected. We found no association with frailty in the very old for CMV sero-positivity, telomere length, markers of oxidative stress or DNA damage and repair. The Fried and Rockwood frailty models measure different albeit overlapping concepts yet biomarker associations were generally consistent between models. Difficulties in operationalizing the Fried model, due to high levels of co-morbidity, limit its utility in the very old.
Publisher
Elsevier Ireland Ltd
URL
http://dx.doi.org/10.1016/j.mad.2012.05.005
DOI
10.1016/j.mad.2012.05.005
PubMed id
22663935
Notes
Collerton, Joanna Martin-Ruiz, Carmen Davies, Karen Hilkens, Catharien M Isaacs, John Kolenda, Claire Parker, Craig Dunn, Michael Catt, Michael Jagger, Carol von Zglinicki, Thomas Kirkwood, Thomas B L Ireland Mech Ageing Dev. 2012 Jun;133(6):456-66. Epub 2012 Jun 1.
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