Elevated Plasma Endothelial Microparticles in Alzheimer’s Disease

• Published in: Dementia and geriatric cognitive disorders Vol. 34; no. 3-4; pp. 174 - 180
• Main Authors: Xue, Shouru, Cai, Xiuyin, Li, Wanjun, Zhang, Zhengchun, Dong, Wanli, Hui, Guozhen
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.01.2012; S. Karger AG
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - blood; Alzheimer Disease - pathology; Alzheimer's disease; Analysis of Variance; Apoptosis - physiology; Biological and medical sciences; Biomarkers - blood; Case-Control Studies; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; E-Selectin - blood; Endothelial Cells - metabolism; Endothelial Cells - pathology; Errors of metabolism; Female; Flow Cytometry; Humans; Lipids (lysosomal enzyme disorders, storage diseases); Male; Medical sciences; Metabolic diseases; Microcirculation - physiology; Middle Aged; Neurology; Neuropsychological Tests; Original Research Article; Platelet Endothelial Cell Adhesion Molecule-1 - blood; Regression Analysis; Republic of Korea; Severity of Illness Index; Cognitive decline; Flow cytometry; Alzheimer’s disease; Endothelial microparticles; Nervous system diseases; Cognitive disorder; Alzheimer disease; Central nervous system disease; Degenerative disease; Alzheimer's disease; Cerebral disorder
• ISSN: 1420-8008; 1421-9824
• DOI: 10.1159/000343491

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.