Abstract
There are clear age-related changes in platelet count and function, driven by changes in hematopoietic tissue, the composition of the blood and vascular health. Platelet count remains relatively stable during middle age (25–60 years old) but falls in older people. The effect of age on platelet function is slightly less clear. The longstanding view is that platelet reactivity increases with age in an almost linear fashion. There are, however, serious limitations to the data supporting this dogma. We can conclude that platelet function increases during middle age, but little evidence exists on the changes in platelet responsiveness in old age (>75 years old). This change in platelet function is driven by differential mRNA and microRNA expression, an increase in oxidative stress and changes in platelet receptors. These age-related changes in platelets are particularly pertinent given that thrombotic disease and use of anti-platelet drugs is much more prevalent in the elderly population, yet the majority of platelet research is carried out in young to middle-aged (20–50 years old) human volunteers and young mice (2–6 months old). We know relatively little about exactly how platelets from people over 75 years old differ from those of middle-aged subjects, and we know even less about the mechanisms that drive these changes. Addressing these gaps in our knowledge will provide substantial understanding in how cell signalling changes during ageing and will enable the development of more precise anti-platelet therapies.
Highlights
Platelets play a vital role in the chronic and acute progression of a range of diseases, most notably cardio-vascular disease (CVD)
As will hopefully become apparent in the course of this review, we know relatively little about how platelets from people over 75 years old differ from those of middle-aged subjects, and we know even less about the mechanisms that drive these changes
Studies in mice confirm that the change in platelet count with age is not restricted to humans
Summary
Platelets play a vital role in the chronic and acute progression of a range of diseases, most notably cardio-vascular disease (CVD). In 2010, % of the 180,000 people who died of CVD in the UK were over years old (British Heart Foundation 2011) It is in this older population that the majority of anti-platelet medication is prescribed, for whom we need to design new well-balanced, effective therapeutic strategies. Age is a major factor giving rise to inter-individual variation in platelet count and function, and is associated with the success of anti-platelet therapy (Biino et al 2011, 2013; Johnson et al 1975; Meade et al 1985b; Mohebali et al 2014; O’Donnell et al 2001; Segal and Moliterno 2006) This effect of ageing is important because most of the work carried out to investigate platelet function, or to design and test new anti-platelet drugs, is performed in young or middle-aged healthy subjects. As will hopefully become apparent in the course of this review, we know relatively little about how platelets from people over 75 years old differ from those of middle-aged subjects, and we know even less about the mechanisms that drive these changes
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