Nehlin 2018 MiP2018

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Aging biomarkers in multimorbidity patients. Nehlin_Presentation

Link: MiP2018

Nehlin JO, Tavenier J, Andersen O (2018)

Event: MiP2018

COST Action MitoEAGLE

We wish to establish clinically-relevant aging biomarkers that can be associated with frailty level and disease state of chronically-ill, multimorbidity elderly patients that will contribute to create an estimate of their current physiological age, serving as a base for personalized treatment interventions.

Gradual accumulation of dysfunctional cells known as senescent cells has been correlated with age-related pathologies in many different types of tissues and organs, and their origin can be explained by various types of damage [1-3]. Cellular senescence is characterized by a series of morphological and physiological changes that ultimately lead to an irreversible state of proliferative arrest and resistance to apoptosis. A major consequence of senescence is the acquisition of a senescence-associated secretory phenotype (SASP) that increases the risk of cancer, inhibits angiogenesis, causes a pro-inflammatory state and alters the normal functioning of tissues, contributing to age-associated pathologies [2,4]. Interestingly, the composition of the SASP appears to vary according to the type of mechanism that induced the senescent state [5-7]. Mitochondria dysfunction can lead to senescence and is characterized by a distinct SASP profile [5,8]. The use of biomarkers of aging can help to reveal the true biological age of an individual [9-12], influenced by epigenetics and resilience-promoting factors [13,14], and could help predict health outcomes in multimorbidity patients. Several biomarker profiles are being analyzed.


Bioblast editor: Plangger M


Labels: Pathology: Aging;senescence 







Affiliations

Clinical Research Center, Copenhagen Univ Hospital-Hvidovre, Denmark. - jan.nehlin@regionh.dk

Support

This project is supported by regional funds from the Capital Region, the Clinical Research Center at Amager and Hvidovre hospitals, the Sofus Carl Emil Friis and Hustru Olga Doris Friis' scholarship and the Toyota Fund.

Figures

Nehlin Figure1 MiP2018.jpg
Figure 1. Design of the FAM-CPH cohort. In dark grey, the FAM-group consists of acutely ill patients aged 65 and over (n=128). In light grey, the Control group consists of citizen matched 1:1 on age, sex and municipality with patients from the FAM-group, but with no recent acute hospital admission (n=54). In italics and arrows, the aspects of biological aging that we will investigate: resilience as the development in aging markers between acute illness and baseline, the biological age as the difference in aging markers between the groups at baseline, the rate of aging as the development in aging markers between baseline and the 1-year follow-up.


Nehlin Figure2 MiP2018.jpg
Figure 2. Example of biomarker analysis in acutely ill elderly patients

Plasma LDH and suPAR levels at admission, n = 91 – significant: p = 0.0003. The tissue-breakdown marker LDH (lactate dehydrogenase 1) [15] and the mortality marker suPAR (soluble urokinase-type plasminogen activator receptor) [16] are predictors of frailty and mortality.








References

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  16. Rasmussen LJ, Ladelund S, Haupt TH, Ellekilde G, Poulsen JH, Iversen K, Eugen-Olsen J, Andersen O (2016) Soluble urokinase plasminogen activator receptor (suPAR) in acute care: a strong marker of disease presence and severity, readmission and mortality. Emerg Med J 33:769-75.