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Dement Geriatr Cogn Disord. 2012;34(3-4):174-80. doi: 10.1159/000343491. Epub 2012 Oct 11.

Elevated plasma endothelial microparticles in Alzheimer's disease.

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  • 1Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou, China.



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.


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.


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.


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.

Copyright © 2012 S. Karger AG, Basel.

[PubMed - indexed for MEDLINE]
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