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Updated: Jun 18, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Platelet activation is caused not by aging but by atherosclerosis
Hitoshi Kurabayashi1, Kazuo Kubota, Akiko Hishinuma
1Department of Medicine, Kusatsu Branch Hospital, Gunma University Hospital, 627-3 Kusatsu, Gunma 377-1711, Japan. hkuraba@saitama-med.ac.jp
Insights
Platelet activation is linked to atherosclerosis, not aging itself. Studies show elderly individuals with atherosclerosis exhibit increased platelet pseudopods and decreased peroxidase, unlike healthy young or non-atherosclerotic elderly subjects.
Area of Science:
- Gerontology
- Hematology
- Cardiovascular Science
Background:
- Platelet activation is known to increase with age.
- It remains debated whether this is due to aging or associated atherosclerosis.
Purpose of the Study:
- To investigate the relationship between platelet activation, aging, and atherosclerosis.
- To differentiate the effects of aging from those of atherosclerosis on platelet function.
Main Methods:
- Examined platelet ultrastructure in young, non-atherosclerotic elderly, and atherosclerotic elderly subjects.
- Assessed platelet shape changes using transmission electron microscopy.
- Quantified peroxidase and fibrinogen content via cytochemical staining and immunogold marking.
Main Results:
- No significant differences in platelet shape, peroxidase, or fibrinogen were found between young and non-atherosclerotic elderly subjects.
- Elderly subjects with atherosclerosis showed increased pseudopod formation and decreased peroxidase content.
- These findings suggest atherosclerosis, not aging, influences platelet activation.
Conclusions:
- Platelet activation is primarily associated with atherosclerosis rather than the aging process itself.
- Distinguishing the independent effects of aging and atherosclerosis on platelets remains challenging.
Abstract:
Platelet activation increases with age, although it is still controversial whether it derives from aging per se or from atherosclerosis concomitant with aging. The purpose of this study is to clarify the association between platelet activation and aging or atherosclerosis. We studied the ultrastructure of platelets in the elderly subjects with or without atherosclerosis and healthy young subjects. The platelet shape changes were evaluated by transmission electron microscopy and the contents of peroxidase and fibrinogen were assessed using a scoring system based on cytochemical staining and immunogold marking methods. No significant differences in platelet shape changes and the contents of peroxidase and fibrinogen in platelet were observed between healthy young and nonatherosclerotic elderly subjects, although the frequency of pseudopods increased and the content of peroxidase decreased in atherosclerotic elderly patients. It is suggested that platelet activation is not derived from aging but from atherosclerosis, although it is difficult to separate aging from coexisting atherosclerosis.
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