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. 2011 Feb;27(1):27-37.
doi: 10.1016/j.cger.2010.08.006.

The biology of aging and frailty

Neal S Fedarko  1
Affiliations

The biology of aging and frailty

Neal S Fedarko. Clin Geriatr Med. 2011 Feb.

Abstract

In developing and validating the concept of frailty as a geriatric syndrome, it has been necessary to distinguish the clinical expression of frailty from normal age-related changes and other age-related disease pathologies. A framework for excluding potentially confounding disease and a working clinical tool to diagnose frailty have been provided. The associations between frailty and other pathophysiologies has also been shown. However, investigating the underlying biologic basis for the geriatric syndrome of frailty by studying basic homeostatic pathways and mechanisms has not proceeded at the same rate. The following article provides an overview of the homeostatic pathways emphasized in research on aging and explains how this science may help to stimulate frailty research.

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Figures

Figure 1
Figure 1
Cellular responses to stressors. Stressors (free radicals, DNA damage, nutrient or oxygen constriction, cell injury; represented by the lightening bolt) challenge cellular homeostasis. The cellular response can be senescence, apoptosis, repair, or neoplastic transformation of the cell. Senescence, a tumor suppressive response is associated with an altered secretory phenotype. The controlled cell death of apoptosis can also be tumor suppressive, though many cells, especially immune cells, normally exit through apoptosis. Apoptosis can, however yield tissue/organ atrophy. Repair enables recovery of homeostasis. In some cases apoptosis is a precursor to repair and recovery (dotted line with arrow). Additionally, the senescent cell phenotype is sometimes a precursor/ contributory to neoplasm formation and cancer progression.
See this image and copyright information in PMC

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