Vascular inflammation in cerebral small vessel disease

Rob P. W. Rouhl*, Jan G. M. C. Damoiseaux, Jan Lodder, Ruud O. M. F. I. H. Theunissen, Iris L. H. Knottnerus, Julie Staals, Leon H. G. Henskens, Abraham A. Kroon, Peter W. de Leeuw, Jan Willem Cohen Tervaert, Robert J. van Oostenbrugge

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


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.
Original languageEnglish
Pages (from-to)1800-1806
JournalNeurobiology of Aging
Issue number8
Publication statusPublished - Aug 2012


  • Lacunar infarcts
  • White matter lesions
  • Adhesion molecules
  • Neopterin
  • Cerebral small vessel disease

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