TY - JOUR
T1 - Vascular inflammation in cerebral small vessel disease
AU - Rouhl, Rob P. W.
AU - Damoiseaux, Jan G. M. C.
AU - Lodder, Jan
AU - Theunissen, Ruud O. M. F. I. H.
AU - Knottnerus, Iris L. H.
AU - Staals, Julie
AU - Henskens, Leon H. G.
AU - Kroon, Abraham A.
AU - de Leeuw, Peter W.
AU - Tervaert, Jan Willem Cohen
AU - van Oostenbrugge, Robert J.
PY - 2012/8
Y1 - 2012/8
N2 - Cerebral small vessel disease (CSVD) is considered to be caused by an increased permeability of the blood-brain barrier and results in enlargement of Virchow Robin spaces (VRs), white matter lesions, brain microbleeds, and lacunar infarcts. The increased permeability of the blood-brain barrier may relate to endothelial cell activation and activated monocytes/macrophages. Therefore, we hypothesized that plasma markers of endothelial activation (adhesion molecules) and monocyte/macrophage activation (neopterin) relate to CSVD manifestations. In 163 first-ever lacunar stroke patients and 183 essential hypertensive patients, we assessed CSVD manifestations on brain magnetic resonance imaging (MRI) and levels of C-reactive protein (CRP), neopterin, as well as circulating soluble adhesion molecules (sICAM-1, sVCAM-1, sE-selectin, sP-selectin). Neopterin, sICAM-1 and sVCAM-1 levels were higher in patients with extensive CSVD manifestations than in those without (p <0.01). Neopterin levels independently related to higher numbers of enlarged Virchow Robin spaces (p <0.001). An inflammatory process with activated monocytes/macrophages may play a role in the increased permeability of the blood brain barrier in patients with CSVD.
AB - Cerebral small vessel disease (CSVD) is considered to be caused by an increased permeability of the blood-brain barrier and results in enlargement of Virchow Robin spaces (VRs), white matter lesions, brain microbleeds, and lacunar infarcts. The increased permeability of the blood-brain barrier may relate to endothelial cell activation and activated monocytes/macrophages. Therefore, we hypothesized that plasma markers of endothelial activation (adhesion molecules) and monocyte/macrophage activation (neopterin) relate to CSVD manifestations. In 163 first-ever lacunar stroke patients and 183 essential hypertensive patients, we assessed CSVD manifestations on brain magnetic resonance imaging (MRI) and levels of C-reactive protein (CRP), neopterin, as well as circulating soluble adhesion molecules (sICAM-1, sVCAM-1, sE-selectin, sP-selectin). Neopterin, sICAM-1 and sVCAM-1 levels were higher in patients with extensive CSVD manifestations than in those without (p <0.01). Neopterin levels independently related to higher numbers of enlarged Virchow Robin spaces (p <0.001). An inflammatory process with activated monocytes/macrophages may play a role in the increased permeability of the blood brain barrier in patients with CSVD.
KW - Lacunar infarcts
KW - White matter lesions
KW - Adhesion molecules
KW - Neopterin
KW - Cerebral small vessel disease
U2 - 10.1016/j.neurobiolaging.2011.04.008
DO - 10.1016/j.neurobiolaging.2011.04.008
M3 - Article
C2 - 21601314
SN - 0197-4580
VL - 33
SP - 1800
EP - 1806
JO - Neurobiology of Aging
JF - Neurobiology of Aging
IS - 8
ER -