Journal
NEUROLOGY
Volume 72, Issue 21, Pages 1858-1863Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181a711f4
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Funding
- Ministry of Science and Technology [SC4120]
- Ministry of Health Welfare [A080448]
- College of Medicine, Seoul National University, South Korea [800-20080511]
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Objective: Neurovascular dysfunction and senescent endothelium contribute to the progression of Alzheimer disease (AD). Circulating angiogenic cells (CACs), such as endothelial progenitor cells (EPCs), provide a cellular reservoir for the endothelial replacement. To study the involvement of CACs in AD pathogenesis, we investigated the levels of CACs in patients with AD. Methods: Consecutive patients with newly diagnosed AD (n = 55), patients with non-AD neurodegenerative diseases (n = 37), and nondemented risk factor control subjects (RF control, n = 55 and 37) were enrolled after matching for age, sex, and Framingham risk score. Peripheral blood samples were taken, and EPC colony-forming units (CFU-EPC) were cultured and counted. Results: The patients with AD had significantly lower CFU-EPC than the RF controls. In the patients with AD, a lower CFU-EPC was independently associated with either a lower Mini-Mental State Examination score or a higher Clinical Dementia Rating scale score, indicating a greater reduction in CFU-EPC in advanced AD. Patients with non-AD neurodegenerative diseases did not show a significant decrease in CFU-EPC levels. Conclusion: Our results indicate that patients with Alzheimer disease (AD) have reduced circulating angiogenic cells, suggesting that an abnormal capacity to regenerate endothelium is associated with AD. Neurology (R) 2009; 72: 1858-1863
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