Platelet function and ageing

• Published in: Mammalian Genome Vol. 27; no. 7-8; pp. 358 - 366
• Main Author: Jones, Chris I.
• Format: Journal Article Book Review
• Language: English
• Published: New York Springer US 01-08-2016; Springer Nature B.V
• Subjects: Aged; Aging - genetics; Aging - pathology; Animal Genetics and Genomics; Animals; Biomedical and Life Sciences; Blood Platelets - metabolism; Blood Platelets - pathology; Cell Biology; Human Genetics; Humans; Life Sciences; Mice; MicroRNAs - genetics; Oxidative Stress - genetics; Platelet Count; Platelet Count; Platelet Production; Hematopoietic Tissue; Platelet Function; Apocynin
• ISSN: 0938-8990; 1432-1777
• DOI: 10.1007/s00335-016-9629-8

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.