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Platelet activation in Alzheimer disease
1Department of Psychiatry, University of Miami School of Medicine, Fla 33136, USA.
Archives of Neurology
|April 30, 1998
Summary
Platelets in Alzheimer disease (AD) patients show increased activation, evidenced by more aggregates and complexes. This heightened platelet activity may play a role in AD pathogenesis.
Area of Science:
- Neuroscience
- Hematology
- Biochemistry
Background:
- Recent studies indicate altered platelet serotonin levels in Alzheimer disease (AD).
- This suggests a potential for increased platelet activation in AD patients.
Purpose of the Study:
- To compare baseline activation of unstimulated platelets in patients with probable AD versus age-matched controls.
Main Methods:
- Flow cytometry assessed platelet activation markers in 91 AD patients and 40 controls.
- Key markers included circulating platelet aggregates, CD62p expression, leukocyte-platelet complexes, and platelet microparticles.
- Analyses controlled for demographic, clinical, and physiological factors.
Main Results:
- AD patients exhibited significantly higher platelet aggregates (39.5% increase), CD62p expression (59.3% increase), and leukocyte-platelet complexes (53.3% increase).
- No significant differences were found in platelet microparticles, platelet count, fibrinogen, or platelet factor 3.
- Platelet activation was independent of disease severity, duration, age, or comorbidities.
Conclusions:
- Platelets from AD patients demonstrate heightened unstimulated activation compared to controls.
- Potential triggers include damaged cerebral endothelial cells or platelet membrane abnormalities.
- Given platelets' role in amyloid precursor protein production, AD platelet activation may influence disease pathogenesis.
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