Frailty Pathophysiology, Phenotype, and Patient Care

Editor(s): R.A. Fielding, C. Sieber, B. Vellas NNI Workshop Series (NNIW) Vol.83 , 2015


Worldwide, the population aged 65 years and more is expected to grow from near 500 million people in 2004 to an estimated 2 billion people by 2050. The geriatric syndrome of frailty is likely to affect a large number of elderly living in the community, as approximately 14% of those are frail and 43% are prefrail based on findings of the Survey of Health, Aging and Retirement in Europe (SHARE) conducted in 10 major European countries.

In a frail state, older adults are at greater risk for adverse outcomes, including falls and admissions to hospitals and nursing homes. Early action is warranted in vulnerable inpiduals because frailty is a predisabled condition, disability is costly, and initiating intervention may modify the frailty trajectory. Yet, today it is more common for older adults to progress to a worsened level of frailty than to transition to an improvement. The development and application of evolving science is important for better patient-centric health care.

  • Cellular Senescence and the Biology of Aging, Disease, and Frailty

    Author(s): N.K. LeBrasseur, T. Tchkonia, J.L. Kirkland

    Population aging simultaneously highlights the remarkable advances in science, medicine, and public policy, and the formidable challenges facing society. Indeed, aging is the primary risk factor for many of the most common chronic diseases and frailty, which result in profound social and economic costs. Population aging also reveals an opportunity, i.e. interventions to disrupt the fundamental biology of aging could significantly delay the onset of age-related conditions as a group, and, as a result, extend the healthy life span, or health span .

    There is now considerable evidence that cellular senescence is an underlying mechanism of aging and age-related conditions. Cellular senescence is a process in which cells lose the ability to pide and damage neighboring cells by the factors they secrete, collectively referred to as the senescence-associated secretory phenotype (SASP). Herein, we discuss the concept of cellular senescence, review the evidence that implicates cellular senescence and SASP in age-related deterioration, hyperproliferation, and inflammation, and propose that this underlying mechanism of aging may play a fundamental role in the biology of frailty.

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