Circulating endothelial progenitor cells and age-related white matter changes.
OBJECTIVE
The objective was to evaluate the relationship between circulating endothelial progenitor cells (EPC) and age-related white matter changes (ARWMC). Endothelial dysfunction plays a role in the development of ARWMC. EPC incorporate into sites endothelial damage and are thought to be involved in the repair of vascular risk factor induced endothelial injury. ARWMC can be evaluated using CT or MRI.


METHODS
In 172 individuals, circulating EPC were defined by the surface markers CD31 and von Willebrand factor. ARWMC were rated on CT scan using the ARWMC scale and divided into 3 groups based on ARWMC scale score (ARWMC score 0 [none], score 1-10 [mild-to-moderate], score >10 [severe]). Severity of ARWMC was correlated with levels of EPC and vascular risk factors.


RESULTS
On univariate analysis, EPC were found to be significantly lower in patients with severe ARWMC (P=0.01). ARWMC were also associated with hypertension (P<0.001), age (P<0.001), creatinine clearance (P=0.031), C-reactive protein (P<0.001), and use of angiotensin-converting enzyme or angiotensin receptor blocker (P=0.004). Multiple logistic regression analysis identified EPC level, age, hypertension, and hypertriglyceridemia as significant independent predictors of severe ARWMC.


CONCLUSIONS
Levels of circulating EPC were significantly lower in patients with severe ARWMC. Other variables significantly associated with severe ARWMC were age, hypertension, and hypertriglyceridemia. Further study is required to delineate the pathophysiological relationship between EPC, vascular risk factors, and ARWMC.
Jickling
Glen
G
Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Canada.
Salam
Abdul
A
Mohammad
Askar
A
Hussain
Muhammad S
MS
Scozzafava
James
J
Nasser
Abdul Majeed
AM
Jeerakathil
Thomas
T
Shuaib
Ashfaq
A
Camicioli
Richard
R
D017677:Age Distribution; D000368:Aged; D000375:Aging / Q000378:metabolism / Q000473:pathology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D001921:Brain / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism; D002452:Cell Count; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D003401:Creatine / Q000378:metabolism; D003704:Dementia / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D018450:Disease Progression; D042783:Endothelial Cells / Q000166:cytology* / Q000502:physiology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications; D015228:Hypertriglyceridemia / Q000150:complications; D008297:Male; D008875:Middle Aged; D018919:Neovascularization, Physiologic / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000473:pathology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism; D012038:Regeneration / Q000502:physiology; D013234:Stem Cells / Q000166:cytology* / Q000502:physiology; D014057:Tomography, X-Ray Computed; D014841:von Willebrand Factor / Q000032:analysis / Q000276:immunology / Q000378:metabolism
D000806:Angiotensin-Converting Enzyme Inhibitors; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C029417:Von Willebrand antigen; D014841:von Willebrand Factor; D002097:C-Reactive Protein; D003401:Creatine