S100B and ADMA in cerebral small vessel disease and cognitive dysfunction

• The expression of S100B and ADMA in SVD was elevated.
• S100B and ADMA were associated with the onset of SVD.
• S100B was a key factor of the disease.
• The patients of SVD had different degrees of cognitive impairment.
• S100B and ADMA were related with cognitive dysfunction of LA.

BackgroundGlial cell activation and endothelial dysfunction are thought to contribute to the pathophysiology of cerebral small vessel disease (SVD). The purpose of the present study was to determine if levels of S100B, a protein highly expressed in glial cells, and asymmetric dimethylarginine (ADMA), which promotes endothelial dysfunction, are elevated in the serum of patients with SVD and correlate with their cognitive functioning.MethodsThe serum levels of S100B and ADMA were measured with enzyme-linked immunosorbent assays in 210 patients with SVD and 207 controls. Cognitive functioning was evaluated using the Montreal Cognitive Assessment. SVD lesions were categorized as isolated lacunar infarcts (ILI), multiple lacunar infarcts, leukoaraiosis (LA), and LA with cerebral atrophy using magnetic resonance imaging.ResultsSVD patients were significantly older, and more likely to have hypertension, diabetes, and heart disease, and smoke compared to controls (Ps < 0.05). Plasma levels of S100B and ADMA were significantly higher in SVD patients (Ps < 0.05), though only S100B was significant after adjusting for the confounding factors. Subtype analyses indicated that ADMA levels were differentially altered depending on lesion type, particularly in cases with ILI and LA (Ps < 0.05). Compared with controls, SVD patients had significant cognitive impairment that was most profound in the cases with LA (all Ps < 0.05). Levels of S100B and ADMA were significantly correlated with cognitive decline in patients with LA (P < 0.05).ConclusionS100B and ADMA are elevated in SVD, and are associated with cognitive impairment in patients with LA lesions.