Nikhil Prasad Fact checked by:Thailand Medical News Team May 31, 2026 43 minutes ago
Medical News: A new study has uncovered an important reason why older adults may remain at higher risk of dangerous blood clots and cardiovascular complications despite taking aspirin. Researchers found that aging appears to increase levels of a key platelet enzyme called cyclooxygenase-1 (Cox-1), leading to greater production of clot-promoting substances and reducing aspirin’s ability to fully suppress platelet activity.
Researchers discover that aging increases platelet Cox-1 levels, potentially reducing aspirin’s ability to prevent
harmful blood clot formation
Scientists Investigate Why Clotting Risk Rises with Age
As people grow older, their risk of heart attacks, strokes, and other cardiovascular problems increases significantly. While doctors have long known that aging is linked to greater blood clotting activity, the biological mechanisms behind this process have remained unclear.
Researchers from the Department of Medical and Cardiovascular Sciences at Sapienza University of Rome, the Department of General Surgery and Surgical Specialty at Sapienza University of Rome, the Department of Internal Medicine, Endocrine and Metabolic Sciences and Infectious Diseases at Azienda Ospedaliero-Universitaria Policlinico Umberto I, the Scientific Institute for Research, Hospitalization and Healthcare IRCCS Neuromed, the Department of Surgery “Paride Stefanini”–Policlinico Umberto I, and the Department of Medical-Surgical Sciences and Biotechnologies at Sapienza University of Rome sought to better understand this phenomenon.
Their investigation focused on patients with atrial fibrillation, a common heart rhythm disorder that substantially increases the risk of stroke and blood clot formation.
Key Enzyme Rises Steadily with Age
The study analyzed 134 patients with atrial fibrillation whose median age was 75 years. Researchers measured blood levels of Cox-1 and thromboxane B2 (TxB2), a stable marker of platelet activation and clotting activity.
The results showed a clear age-related trend. Both Cox-1 and TxB2 levels increased progressively as patients got older. Statistical analysis revealed that older age was strongly associated with higher Cox-1 levels and higher TxB2 production.
Importantly, researchers found that Cox-1 appeared to explain roughly half of the relationship between aging and increased thromboxane production. This suggests that rising Cox-1 activity is a major biological driver of age-related platelet hyperactivity.
For ordinary people, this means that the blood-clotting machinery becomes increasingly active with age, even when other medical conditions and treatments are taken into account.
Why This Matters for Aspirin Therapy
Aspirin works primarily by blocking Cox-1, preventing platelets from producing thromboxane and reducing their ability to form clots.
To determine whether aging affects aspirin responsiveness, the researchers performed additional laboratory experiments using platelets collected from younger and older participants.
The findings were striking.
In participants younger than 65 years, aspirin progressively reduced thromboxane production as doses increased. However, in participants aged 65 years and older, aspirin's inhibitory effects were much weaker.
The researchers discovered that older individuals had significantly higher levels of platelet Cox-1 protein. The more Cox-1 that was present, the less effective aspirin became at suppressing thromboxane production.
This suggests that aging may create a situation in which platelets produce so much Cox-1 that standard aspirin treatment struggles to completely shut down the clotting pathway.
A Possible Explanation for Aspirin Resistance
The findings may help explain a phenomenon often referred to as "aspirin resistance," where some individuals continue to show platelet activity despite taking aspirin.
Previous clinical studies have reported that aspirin provides less cardiovascular protection in many elderly individuals than expected. Some recent large studies have even questioned the benefit of aspirin for primary prevention in older adults because the reduction in cardiovascular events may not outweigh bleeding risks.
This
Medical News report highlights that elevated Cox-1 expression could be one of the biological reasons behind this reduced effectiveness. The discovery provides a new mechanistic explanation for why older adults may remain vulnerable to clot-related complications despite aspirin therapy.
What the Researchers Concluded
The researchers concluded that aging is associated with a substantial increase in platelet Cox-1 expression and thromboxane production. As Cox-1 levels rise, platelets become more active and increasingly difficult for aspirin to suppress.
These findings suggest that age-related changes in platelet biology may contribute to the reduced effectiveness of aspirin observed in many older adults.
The scientists emphasized that additional studies are needed to determine exactly why Cox-1 increases with age and whether new treatment strategies could better control platelet activity in elderly patients. If confirmed in larger studies, the findings could eventually influence how antiplatelet therapies are selected and optimized for aging populations, particularly those with atrial fibrillation and other cardiovascular conditions where clot prevention remains a major clinical challenge.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/11/4972
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