Platelets are specialized effector cells that rapidly respond to sites of vascular injury. However, emerging data demonstrate that platelets possess diverse functions that also mediate inflammatory responses and neurological diseases. These functions are relevant to disease processes prevalent among older adults and likely influence susceptibility to thrombotic and inflammatory disorders.
Platelet counts decrease in aged individuals whereas platelet reactivity increases. The platelet transcriptome is altered in aged individuals resulting in altered platelet function and exaggerated inflammation. Platelet signaling to monocytes in aging results in significantly more cytokines because of increased platelet-derived granzyme A. Platelet activation in aging appears to be driven, in part, because of increased reactive oxygen species and activation of the mammalian target of rapamycin pathway. Increased platelet hyperactivity in diseases is associated with aging, such cardiovascular disease and sepsis, exaggerate inflammation and thrombosis. Noncanonical functions of platelets influence the development of neurological diseases including Alzheimer's disease.
Although there have been advances dissecting the molecular mechanisms regarding aging-related changes in platelets, many knowledge gaps still remain. Studies filling these gaps are likely to identify new mechanisms driving aging-related changes in platelet gene expression and function, and contributing to injurious thrombo-inflammation in older adults.
aUniversity of Utah Molecular Medicine Program
bDepartment of Internal Medicine, University of Utah
cDepartment of Internal Medicine and GRECC, George E. Wahlen VAMC, Salt Lake City, Utah, USA
Correspondence to Robert A. Campbell, PhD, Assistant Professor of Medicine, University of Utah Health Sciences Center, Eccles Institute of Human Genetics, 15 North 2030 East, Bldg 533, Suite 4220, Salt Lake City, Utah 84112, USA. Tel: +1 801 585 0950; fax: +1 801 585 0701; e-mail: firstname.lastname@example.org