Platelets are essentially structured chunks of cytoplasm shed by the megakaryocyte cells responsible for producing them, released into the blood stream. They are important in blood clotting and the innate immune response. Inappropriate blood clot formation known as thrombosis occurs more readily in later life, but it is unclear as to the degree to which age-related changes in platelets, versus other systems, are important to this process, or where platelets sit in the complex chains of cause and effect. The open access paper noted here reviews what is known of the aging of platelets and related mechanisms, a topic that is not as well investigated as other aspects of cardiovascular aging.
Platelet count is inversely associated with age. A large study based on the Third National Health and Nutrition Examination Survey including 12,142 American subjects showed a significant decrease of 10 × 10^3 platelets/μL in individuals in the 60-69 year age group as compared with those between the ages of 20-59 years, and of 20 × 10^3 platelets/μL in patients aged over 69 years of age, after adjusting for many covariates such as nutritional deficiencies, medication, inflammatory conditions, autoimmune or viral illnesses, and consumption of alcohol and tobacco. This suggests that the drop in platelet count with age is part of the biological aging process per se and not only due to environmental factors.
One of the most documented changes in platelet function during aging is platelet hyperactivity. Bleeding time decreases significantly in aging, denoting a faster clot formation and indirectly an enhanced platelet activity in the elderly. Furthermore, platelets from older men and women have a greater sensitivity to aggregation induced by classical agonists. Furthermore, β-thromboglobulin and platelet factor 4 (PF4), two proteins secreted from platelets α-granules, are both found at a significantly higher level in plasma of older compared with younger subjects. This is consistent with the hyperaggregability observed in elderly individuals since platelets release their granule content during activation.
The mechanisms of this age-related platelet hyperactivity remain unclear. Researchers have tested the hypothesis that modifications in phosphoinositide turnover, an important signaling mechanism of platelet activation, may be responsible for platelet hyperactivity in aging. They have found that platelet phosphoinositide turnover is enhanced in aging and correlates positively with platelet aggregation and plasma β-thromboglobulin levels. It has also been suggested that there could be a functional or expressional change in platelet α and β-adrenoreceptors, however the reported literature is conflicting.