BACKGROUND/AIMS: Endothelial microparticles (EMPs) in plasma are elevated in several vascular diseases. Alzheimer's disease (AD) is associated with microcirculatory injury, capillary blocking and disruption of the blood-brain barrier. We wanted to test the hypothesis that EMPs would be increased in AD patients and would correlate with a cognitive decline, and to determine if EMPs are released as a result of activation or apoptosis/necrosis in AD. METHODS: EMP levels in plasma of AD patients and controls were quantified by flow cytometry. EMP markers for apoptosis/necrosis [platelet/endothelial cell adhesion molecule-1 (PECAM-1)/CD31] and for activation (E-selectin/CD62e) were evaluated. The EMP CD62E/CD31 populations ratio of ≤1.0 was used to differentiate activation from apoptosis. RESULTS: Significantly higher CD31+/CD42- and CD62e+/CD42- counts were observed in the AD group relative to the controls (p < 0.05). There was no difference between the moderate- to-severe AD group and the mild AD group. Significant correlations were found between circulating EMP counts and Mini-Mental State Examination and AD Assessment cognition (ADAS-cog) score. Multivariate regression analysis demonstrated the persistence of significant correlations between ADAS-cog score and CD31+/CD42- EMPs. CONCLUSION: The (PECAM-1)/CD31 ratio demonstrated that EMPs were generated via apoptosis/necrosis and not by activation. Certain circulating EMP phenotypes may be associated with a cognitive decline of AD patients. EMP analysis shows a promising contribution to understanding vascular pathophysiology in AD.
BACKGROUND/AIMS: Endothelial microparticles (EMPs) in plasma are elevated in several vascular diseases. Alzheimer's disease (AD) is associated with microcirculatory injury, capillary blocking and disruption of the blood-brain barrier. We wanted to test the hypothesis that EMPs would be increased in ADpatients and would correlate with a cognitive decline, and to determine if EMPs are released as a result of activation or apoptosis/necrosis in AD. METHODS: EMP levels in plasma of ADpatients and controls were quantified by flow cytometry. EMP markers for apoptosis/necrosis [platelet/endothelial cell adhesion molecule-1 (PECAM-1)/CD31] and for activation (E-selectin/CD62e) were evaluated. The EMP CD62E/CD31 populations ratio of ≤1.0 was used to differentiate activation from apoptosis. RESULTS: Significantly higher CD31+/CD42- and CD62e+/CD42- counts were observed in the AD group relative to the controls (p < 0.05). There was no difference between the moderate- to-severe AD group and the mild AD group. Significant correlations were found between circulating EMP counts and Mini-Mental State Examination and AD Assessment cognition (ADAS-cog) score. Multivariate regression analysis demonstrated the persistence of significant correlations between ADAS-cog score and CD31+/CD42- EMPs. CONCLUSION: The (PECAM-1)/CD31 ratio demonstrated that EMPs were generated via apoptosis/necrosis and not by activation. Certain circulating EMP phenotypes may be associated with a cognitive decline of ADpatients. EMP analysis shows a promising contribution to understanding vascular pathophysiology in AD.