CAP2 Expression Correlates with Frailty, Not Chronological Age

CAP2 is involved in maintenance of the actin cytoskeleton of cells, and as such is one of those proteins whose function might indirectly affect near every process of interest in the cell. It is known to be necessary to heart contractility and the actin remodeling observed in neurons, for example. That makes it a little hard to speculate usefully as to why decreased expression might be correlated with frailty in humans, particularly given that expression doesn't otherwise appear to fall with age, and the authors of this epidemiological study don't make much of an attempt at a hypothesis. Current knowledge of CAP2 is the starting point for a thread of investigation that may last a good many years.

Frailty is a geriatric syndrome that results from multisystem impairment caused by age-associated accumulation of deficits. The frailty index is used to define the level of frailty. Several studies have searched for molecular biomarkers associated with frailty, to meet the needs for personalized care. Cyclase-associated protein 2 (CAP2) is a multifunctional actin-binding protein involved in various physiological and pathological processes, that might reflect frailty's intrinsic complexity.

This study aimed to investigate the association between frailty index and circulating CAP2 concentration in 467 community-dwelling older adults (median age: 79; range: 65-92 years). The selected robust regression model showed that circulating CAP2 concentration was not associated with chronological age, as well as sex and education. However, circulating CAP2 concentration was significantly and inversely associated with the frailty index: a 0.1-unit increase in frailty index leads to ~0.5-point mean decrease in CAP2 concentration. Furthermore, mean CAP2 concentration was significantly lower in frail participants (i.e., frailty index ≥0.25) than in non-frail participants.

This study shows the association between serum CAP2 concentration and frailty status for the first time, highlighting the potential of CAP2 as a biomarker for age-associated accumulation of deficits.