Qiang Gao1, Ying Fan2, Lu-Yan Mu3, Lan Ma4, Zhi-Qiang Song4, Yi-Na Zhang5. 1. Department of Geriatrics, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Key Laboratory of Myocardial Ischemia Mechanism and Treatment Ministry, Harbin 150086, China. 2. Department of Geriatrics, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Electronic address: fanyingyan@163.com. 3. Department of Neurosurgery, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China. 4. Department of Geriatrics, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. 5. Department of Geriatrics, Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Electronic address: yinazhlu@163.com.
Abstract
BACKGROUND: Glial 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. METHODS: The 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. RESULTS: SVD 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). CONCLUSION: S100B and ADMA are elevated in SVD, and are associated with cognitive impairment in patients with LA lesions.
BACKGROUND: Glial 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. METHODS: The 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. RESULTS:SVDpatients 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 SVDpatients (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, SVDpatients 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). CONCLUSION:S100B and ADMA are elevated in SVD, and are associated with cognitive impairment in patients with LA lesions.
Authors: A Wallin; E Kapaki; M Boban; S Engelborghs; D M Hermann; B Huisa; M Jonsson; M G Kramberger; L Lossi; B Malojcic; S Mehrabian; A Merighi; E B Mukaetova-Ladinska; G P Paraskevas; B O Popescu; R Ravid; L Traykov; G Tsivgoulis; G Weinstein; A Korczyn; M Bjerke; G Rosenberg Journal: BMC Neurol Date: 2017-05-23 Impact factor: 2.474
Authors: Zsófia Hoyk; Melinda E Tóth; Nikolett Lénárt; Dóra Nagy; Brigitta Dukay; Alexandra Csefová; Ágnes Zvara; György Seprényi; András Kincses; Fruzsina R Walter; Szilvia Veszelka; Judit Vígh; Beáta Barabási; András Harazin; Ágnes Kittel; László G Puskás; Botond Penke; László Vígh; Mária A Deli; Miklós Sántha Journal: Front Cell Neurosci Date: 2018-10-25 Impact factor: 5.505
Authors: Vladimir A Parfenov; Olga D Ostroumova; Tatiana M Ostroumova; Alexey I Kochetkov; Victoria V Fateeva; Kristina K Khacheva; Gulnara R Khakimova; Oleg I Epstein Journal: Neuropsychiatr Dis Treat Date: 2019-05-21 Impact factor: 2.570
Authors: Francesco Janes; Adriana Cifù; Maria Elena Pessa; Rossana Domenis; Gian Luigi Gigli; Nova Sanvilli; Annacarmen Nilo; Riccardo Garbo; Francesco Curcio; Roberta Giacomello; Martina Fabris; Mariarosaria Valente Journal: Sci Rep Date: 2019-10-02 Impact factor: 4.379
Authors: Jiaxin Guan; Chaoqi Yan; Qiang Gao; Jun Li; Li Wang; Ming Hong; Xiuhai Zheng; Zhiqiang Song; Mei Li; Meiling Liu; Ying Fan; Lan Ma Journal: Medicine (Baltimore) Date: 2017-02 Impact factor: 1.817